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Baba immunisering

Baba immunisering


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Ek weet dat polio-entstof bestaan ​​uit 'n klein dosis poliovirus self, wat die liggaam se immuniteit teen die siekte aktiveer. 'n Baba kry 'n aantal entstowwe, insluitend waterpokkies, tetanus, difterie, ens., sien hier vir besonderhede. Werk al hierdie entstowwe volgens dieselfde beginsel, dit wil sê hulle bevat 'n klein dosis van die onderskeie virus/bakterieë om gashere se immuniteit te aktiveer?


Daar is 'n wye verskeidenheid verskillende soorte entstowwe. Die basiese beginsel is dat die menslike (en meer algemeen, gewerwelde kakebeen) immuunstelsel indringers kan identifiseer deur gedeeltes van makromolekules op daardie indringers wat antigene genoem word, te herken en daarop te reageer. Entstowwe gebruik hierdie beginsel deur die immuunstelsel voor die tyd aan spesifieke antigene bloot te stel, sodat die immuunstelsel daarvoor voorberei word. Daar is natuurlik baie meer besonderhede oor hoekom dit nuttig is, maar ek dink dit is buite die bestek van hierdie vraag.

polio-entstof bestaan ​​uit klein dosis poliovirus self

Entstowwe behels gewoonlik nie 'n klein hoeveelheid van die patogeen self nie. Huidige poliovirus-entstowwe sluit in 'n geïnaktiveerde virus (gedood met formaldehied) wat nie kan voortplant nie, en verskeie lewende verswakte virusse, dit is verskillende stamme van virusse wat kan repliseer, maar nie siektes veroorsaak nie. Die geïnaktiveerde virus word in die Verenigde State gebruik, maar die verswakte virus word in sommige ander lande gebruik.

Daar is verskeie soorte entstowwe, en nie een van hulle behels klein dosisse van die patogeen self nie. Die sleutel hier is om die immuunstelsel aan die antigeen bloot te stel, nie die patogeen nie. Soos met polio, is die hoofgroepe lewende verswakte of geïnaktiveerde entstowwe. Daar is baie soorte geïnaktiveerde entstowwe. Hulle kan heel doodgemaakte virusse of bakterieë wees, of net die belangrike dele. Sommige entstowwe is 'n net-subset van sleutelproteïene of polisakkariede.

Jy kan lees oor al hierdie besonderhede in die CDC pienk boek. Hoofstuk 1 bespreek die beginsels en die verskillende tipes entstowwe. Hoofstuk 18 bespreek poliovirus.


Klein dosis óf gedood óf lewende verswakte (hulle word in ander diere gekweek, so hulle ontwikkel om daardie dier beter te besmet, wat hulle stadiger maak om mense te besmet) patogeen ... ja, dit is die algemene idee agter alle inenting.


Baba-immunisering - Biologie

Om 'n ouer te wees is 'n groot verantwoordelikheid met baie besluite oor hoe om jou kinders die beste te beskerm, soos hoe om die huis baba te beskerm en wanneer om na 'n stootstoeltjie oor te skakel. Maar nie alle bedreigings vir jou kinders’ se veiligheid is sigbaar nie.

Entstowwe help om aansteeklike siektes te voorkom wat eens baie kinders doodgemaak of ernstig benadeel het. Sonder entstowwe is jou kinders in gevaar vir ernstige siektes, insluitend masels, pampoentjies, kinkhoes en griep, wat kan lei tot ongeskiktheid of selfs die dood. Selfs hier in die Verenigde State word babas en jong kinders gereeld die slagoffers van hierdie ernstige, lewensgevaarlike siektes, soos kinkhoes en masels.

Die beste ding wat jy kan doen om jou kinders voor te berei vir 'n gesonde lewe, is om die feite oor inentings te leer en seker te maak dat hulle hul entstowwe betyds ontvang. Kyk na ons nuwe Moenie oorslaan nie veldtog wat praat oor die belangrikheid daarvan om enige inentings wat u gesin tydens die pandemie gemis het, in te haal.

Hoekom moet ek my kind inent?

As ouer wil jy jou kleinding teen skade beskerm. En deur middel van entstowwe het jy die mag om jou kinders teen 14 gevaarlike siektes deur die ouderdom van 2 te beskerm. Trouens, entstowwe voorkom ongeveer 10,5 miljoen gevalle van aansteeklike siektes per jaar en red 33 000 lewens in die Verenigde State alleen. Sonder die beskerming wat entstowwe bied, bly jou kinders kwesbaar vir gevaarlike siektes.


Genetika beïnvloed hoe beskermende kinderjare-entstowwe vir individuele babas is

Krediet: CC0 Public Domain

'n Genoomwye soektog onder duisende kinders in die VK en Nederland het genetiese variante aan die lig gebring wat verband hou met verskillende vlakke van beskermende teenliggaampies wat na roetine-inentings vir kinders geproduseer word. Die bevindinge, wat 11 Junie in die joernaal verskyn Selverslae, kan die ontwikkeling van nuwe entstofstrategieë inlig en kan lei tot gepersonaliseerde inentingskedules om entstofdoeltreffendheid te maksimeer.

"Hierdie studie is die eerste wat 'n genoomwye genotiperingbenadering gebruik, wat 'n paar miljoen genetiese variante beoordeel, om die genetiese determinante van immuunreaksies op drie roetine-entstowwe vir kinders te ondersoek," sê Daniel O'Connor van die Universiteit van Oxford, wat mede is. -eerste skrywer op die vraestel saam met Eileen Png van die Genome Institute of Singapore. "Terwyl hierdie studie 'n goeie begin is, toon dit ook duidelik dat meer werk nodig is om die komplekse genetika wat betrokke is by entstofreaksies volledig te beskryf, en om hierdie doel te bereik sal ons baie meer individue moet bestudeer."

Entstowwe het 'n rewolusie in openbare gesondheid veroorsaak en miljoene sterftes elke jaar voorkom, veral in die kinderjare. Die handhawing van teenliggaampies in die bloed is noodsaaklik vir voortgesette entstof-geïnduseerde beskerming teen patogene. Tog is daar aansienlike variasie in die omvang en volharding van entstof-geïnduseerde immuniteit. Boonop neem teenliggaampies vinnig af na immunisering met sekere entstowwe in die vroeë babajare, so boosters is nodig om beskerming te handhaaf.

"Om robuuste en volgehoue ​​entstof-geïnduseerde immuniteit van vroeë lewe op te roep, is 'n deurslaggewende komponent van globale gesondheidsinisiatiewe om die las van aansteeklike siektes te bekamp," sê O'Connor. "Die meganismes onderliggend aan die volharding van teenliggaampies is van groot belang, aangesien die doeltreffendheid en aanvaarbaarheid van entstowwe verbeter sal word as beskerming na baba-immunisering volgehou word sonder dat dit nodig is vir herhaaldelike hupstoot deur die kinderjare."

Entstofreaksies en die volharding van immuniteit word bepaal deur verskeie faktore, insluitend ouderdom, geslag, etnisiteit, mikrobiota, voedingstatus en aansteeklike siektes. Tweelingstudies het ook getoon dat entstofgeïnduseerde immuniteit hoogs oorerflik is, en onlangse studies het begin om die genetiese komponente onderliggend aan hierdie komplekse eienskap te ontkies.

Om genetiese faktore te ondersoek wat die volharding van immuniteit bepaal, het O'Connor en kollegas 'n genoomwye assosiasiestudie van 3 602 kinders in die VK en Nederland uitgevoer. Die navorsers het gefokus op drie roetine-entstowwe vir kinders wat teen lewensgevaarlike bakteriële infeksies beskerm: kapsulêre groep C meningokokke (MenC), Haemophilus influenzae tipe b (Hib), en tetanus toksoïed (TT) entstowwe. Hulle het ongeveer 6,7 miljoen genetiese variante ontleed wat 'n enkele DNS-boublok, bekend as enkelnukleotiedpolimorfismes (SNP's), wat verband hou met entstof-geïnduseerde teenliggaampies in die bloed, ontleed.

Die navorsers het twee genetiese lokusse geïdentifiseer wat verband hou met die volharding van entstofgeïnduseerde immuniteit na kinderimmunisering. Die volharding van MenC-immuniteit word geassosieer met SNP's in 'n genomiese streek wat 'n familie van seinregulerende proteïene bevat, wat betrokke is by immunologiese sein. Intussen word die volharding van TT-spesifieke immuniteit geassosieer met SNP's in die menslike leukosietantigeen (HLA) lokus. HLA-molekules bied peptiede aan T-selle, wat op hul beurt B-selle veroorsaak om teenliggaampies te produseer.

Hierdie variante is waarskynlik verantwoordelik vir slegs 'n klein gedeelte van die genetiese determinante van volharding van entstof-geïnduseerde immuniteit. Boonop is dit onduidelik of die bevindinge van toepassing is op ander etniese bevolkings behalwe Kaukasiërs van die VK en Nederland. Maar volgens die skrywers kan neonatale siftingsbenaderings binnekort genetiese risikofaktore insluit wat die volharding van immuniteit voorspel, wat die weg baan vir persoonlike entstofregimes.

"Ons doen nou in-diepte ondersoeke na die biologie van die genetiese variante wat ons in hierdie studie beskryf het," sê O'Connor. "Ons het ook verdere navorsing beplan, in groter groepe kinders en ander bevolkings wat by inenting baat vind, om ons begrip te bevorder van hoe ons genetiese samestelling entstofreaksies vorm."


Ontwikkelingsbiologie van die aangebore immuunrespons: implikasies vir neonatale en baba-entstofontwikkeling

Molekulêre karakterisering van meganismes waardeur menslike patroonherkenningsreseptore (PRR's) gevaarseine opspoor, het ons begrip van die aangebore immuunstelsel aansienlik uitgebrei. PRR's sluit in Tol-agtige reseptore, nukleotied-oligomerisasie domein-agtige reseptore, retinoïensuur-induseerbare geen-agtige reseptore, en C-tipe lektien reseptore. Karakterisering van die ontwikkelingsuitdrukking van hierdie sisteme in die fetus, pasgebore baba en baba is onvolledig, maar het belangrike insigte oor neonatale vatbaarheid vir infeksie opgelewer. Aktivering van PRR's op antigeen-presenterende selle verhoog die koste-stimulerende funksie, en dus is PRR-agoniste potensiële entstofhulpmiddels, waarvan sommige reeds in kliniese gebruik is. Studie van PRR'e het dus ook aan die lig gebring hoe voorheen geheimsinnige immunomoduleerders hul aksies kan bemiddel, insluitend die entstof-adjuvans aluminiumhidroksied wat 'n sitosoliese proteïenkompleks bekend as die Nacht-domein, leucienryke herhaling en piriendomein-bevattende proteïen 3-inflammasoom aktiveer wat lei tot interleukien-1β produksie. Vordering met die karakterisering van PRR'e is dus die inlig en uitbreiding van die ontwerp van verbeterde byvoegmiddels. Hierdie oorsig gee 'n opsomming van onlangse ontwikkelings op die gebied van aangebore immuniteit wat die ontwikkelingsuitdrukking in die fetus, pasgebore en baba beklemtoon en die implikasies daarvan vir die ontwerp van meer effektiewe neonatale en baba-entstowwe.

Behoefte aan effektiewe neonatale en baba-entstowwe

Op 'n wêreldbasis lei infeksies tot ~ 2 miljoen sterftes per jaar in diegene jonger as 6 maande (Wêreldgesondheidsorganisasie) (1). Algemene patogene by pasgeborenes en/of babas sluit in Gram-positiewe bakterieë (bv., groep B streptokokke, Streptococcus pneumoniae), Gram-negatiewe bakterieë (soos Escherichia coli en Bacillus pertussis), herpes simplex-virus, respiratoriese sinsitiale virus en rotavirus. Hierdie vatbaarheid beklemtoon die onvervulde behoefte aan effektiewe entstowwe vir pasgeborenes en babas en die funksionele immuniteitsgebreke wat oorkom moet word in die ontwerp van entstowwe wat die kleintjies voldoende beskerm. Aangesien geboorte die mees betroubare punt van gesondheidsorgkontak wêreldwyd is, is entstowwe wat by geboorte aktief is 'n belangrike globale gesondheidsvereiste (2). Ontwerp en ontwikkeling van sulke entstowwe sal begrip vereis van die ontwikkelingsuitdrukking van aangebore immuunweë waarvan die aktivering die aanpasbare immuunrespons versterk.

Afsonderlike aspekte van neonatale aangebore immuniteit wat uitdagings inhou vir effektiewe inenting vroeg in die lewe

Die fetale immuunstelsel is sterk Th2-bevooroordeeld, vermoedelik om pro-inflammatoriese Th1-tipe allo-immuunreaksies op moederweefsel te vermy wat premature geboorte of spontane aborsie kan veroorsaak.

Geboorte veroorsaak 'n dramatiese verandering in die omgewing wat verdere eise aan die neonatale immuunstelsel stel, wat die oorgang van 'n normaalweg steriele intra-uteriene kompartement na 'n vreemde antigeen (Ag)-ryke eksterne omgewing bemiddel. Hierdie oorgang sluit die eerste kolonisasie van die vel en spysverteringskanaal in. In teenstelling met lae vlakke van Th1-tipe sitokiene [bv., tumornekrosefaktor (TNF), interleukien (IL)-12p70, interferon (IFN)-γ], menslike neonatale plasma bevat hoë vlakke van die Th2-tipe sitokien IL-6 in vivo by geboorte en dwarsdeur die eerste week van die lewe (3). IL-6 veroorsaak 'n akute fase reaksie by geboorte wat kan dien om te beskerm teen bakteriële infeksies en duidelike mikrobiese produkte en / of patroonherkenning reseptor (PRR) agoniste (4).

Die duidelike polarisasie van fetale en vroeë neonatale immuunresponse bied struikelblokke vir effektiewe neonatale immunisering, insluitend verswakte antigeen-presenterende sel (APC) response (bv., verswakte IFNγ-produksie) vir baie (maar nie alle nie) stimuli, 'n Th2-vooroordeel vir immuunresponse, verswakte teenliggaam (Ab) affiniteitsrypwording (5), en die potensiële inhiberende effek van moederlike Abs (6).

Kwantitatiewe en kwalitatiewe verskille bestaan ​​tussen neonatale en volwasse APC's. Kwalitatiewe verskille is duidelik in menslike monosiete in utero soos geassesseer deur vloeisitometrie wat verminderde uitdrukkingsvlakke van groot histoversoenbaarheidskompleks (MHC) klas II-molekules aandui (7). Verskeie meganismes is geïmpliseer om neonatale APC's na Th2-tipe reaksies te skeef, insluitend a) die produksie deur plasentale weefsels van transformerende groeifaktor-β, progesteroon en prostaglandien E2 wat Th2 sitokienproduksie verhoog (8) en b) die teenwoordigheid in neonatale bloed plasma van relatief hoë konsentrasies (~ 300 nM) van adenosien, 'n immuunonderdrukkende endogene purienmetaboliet (4,9). Die patrone van neonatale sitokienproduksie blyk relevant te wees in vivo, deurdat menslike neonatale perifere serumvlakke van TNF na geboorte, gedurende die eerste week van die lewe, laag bly (relatief tot menslike volwasse serum), terwyl vlakke van IL-6, 'n Th2-polariserende sitokien met anti-inflammatoriese eienskappe, toeneem.

Veelvuldige studies dokumenteer dat menslike neonatale monosiete en APC's suboptimaal funksioneer wanneer dit getoets word in vitro met betrekking tot koste-stimulerende reaksies op die meeste stimuli (10). Studies van muriene neonatale dendritiese selle (DC's) het getoon dat Ag-aanbieding toeneem tydens ontogenie, wat verband hou met verhoogde ko-stimulerende molekule-uitdrukking en verhoogde reaksies op proteïen-gekonjugeerde, T-sel-afhanklike polisakkaried Ags (11). C57BL/6 neonatale muise (1–7 d) het egter sterker LPS-geïnduseerde inflammatoriese sitokienproduksie deur splenosiete in die teenwoordigheid van T-selle getoon in vitro en na intraperitoneale inspuiting in vivo, toegeskryf aan neonatale kwantitatiewe tekort aan CD4 + en CD8 + T-selle (12). Dus, inflammatoriese reaksies in neonate blyk afhanklik te wees van die spesie [let op dat aangebore immuungene hiperveranderlik is tussen spesies, insluitend tussen mense en muise (13,14)], eksperimentele model (in vitro versus in vivo), ekstrasellulêre kultuurmedium [outoloog 100% (vol/vol) adenosienryke neonatale plasma/serum (15) versus lae konsentrasies van hitte-geïnaktiveerde fetale kalfserum wat in baie studies gebruik word], en spesifieke stimulus bestudeer.

In teenstelling met neonatale APC's, is neonatale CD4 + /CD25 hoë T regulatoriese selle (Treg) ten volle funksioneel en word in 'n hoë oorvloed in menslike fetale limfoïede weefsel (16) en pasgebore naelstringbloed (17,18) aangetref. Neonatale Treg-selle onderdruk beide T-responder-selproliferasie en Th1-sitokien (bv., IFN-γ) produksie, geïnduseer deur self-Ags, om aanpasbare immuunresponse te beperk. Treg bemiddel hul effekte deur beide selkontakafhanklike en kontak-onafhanklike meganismes, insluitend afskeiding van IL-10, CD39 en CD73 (ektonukleotidase)-gemedieerde generasie van ekstrasellulêre adenosien, en adenosien A2A-reseptor-gemedieerde verbetering van sikliese AMP-konsentrasies in teiken T-responderselle (19,20). Neonatale inhibisie van outo-immuniteit via Treg-onderdrukking het duidelike voordele aangesien neonate die eerste keer die vreemde-Ag-ryk wêreld teëkom, maar hierdie effekte kan nadelig wees vir neonatale immuniteit teen infeksie (21) en vir neonatale entstofreaksies (22,23).

Aangebore immuunaktivering verhoog aanpasbare immuunresponse

Aktivering van PRR's op APC's soos makrofage en DC's verhoog Ag-presenterende aktiwiteit en aanpasbare immuunresponse via direkte en indirekte meganismes (24). PRR-sein word beïnvloed deur kruisseine wat bemiddel word via diverse PRR klasse, tyrosine kinases, tyrosine fosfatases, ubiquitinating stelsels, en glukokortikoïede, en dus wissel tussen verskillende sel tipes (25). Met aktivering verwerk en bied DC's Ags doeltreffend aan in die konteks van MHC, verhoog die produksie van Th1-polariserende sitokiene soos IL-12p70, en reguleer kostimulerende molekules op (bv., CD40, CD80, CD86) en chemokienreseptore wat selmigrasie van die weefsels na die dreinerende limfknope bemiddel. Sodra dit binne die limfknope is, tree DC's in wisselwerking met naïewe T- en B-selle wat hul differensiasie in effektorselle veroorsaak, en sodoende 'n verworwe immuunrespons veroorsaak.

Benewens hul direkte effek op APC's, verbeter PRR-agoniste ook die oorgang van aangebore na aanpasbare immuunresponse via indirekte meganismes. Byvoorbeeld, tol-agtige reseptor (TLR)-gemedieerde DC-aktivering induseer IL-6 wat T-responder selle onweerstaanbaar maak teen inhibisie deur onderdrukkende Treg (26). Weefsel-afgeleide seine kan ook APC's beïnvloed en die tipe effektorklas wat gegenereer word, beheer (27). TLR-gemedieerde aktivering van DC's verbeter limfknoopfunksie via sneller DC-migrasie na limfknope, uitdrukking van vaskulêre endoteelgroeifaktor, verhoging van hoë endoteelvenuleproliferasie, hermodellering van primêre voerarterioles, en verhoging van nodale bloedvloei en werwing van seldsame Ag-spesifieke limfosiete (28,29).

Die indrukwekkende vordering met die definisie van die potensiële rolle van PRR's het 'n geleentheid gebied om die ontwikkeling van aangebore immuunresponse na geboorte beter te verstaan, met potensiële implikasies vir die optimalisering van entstofontwikkeling. Later hersien ons die huidige stand van kennis met betrekking tot die ontwikkelingsuitdrukking van sleutel PRR's, en beklemtoon beide onlangse vordering en leemtes in ons kennis.

Ontwikkelingsuitdrukking van PRR's

Reaksies op mikrobiese infeksie word geïnisieer deur 'n aangebore immuunstelsel wat verskillende PRR's bevat wat gereed is vir aktivering in ekstrasellulêre en intrasellulêre liggings (Fig. 1).

Meganismes van aangebore immuunaktivering wat deur entstofhulpmiddels geïnduseer word. TLR-agoniste wat in verskeie neonatale entstowwe gevind word (Tabel 1) aktiveer óf selgeassosieerde óf intrasellulêr geleë TLR'e of NOD's. Hierdie PRR's reageer dan met spesifieke adaptermolekules wat uitloop op NF-KB- of IRF-aktivering. Virale-afgeleide produkte (dsRNA of ssRNA) kan ook endosomale TLRs aktiveer, saam met RLRs (soos RIG-I), wat tipe I IFN-produksie veroorsaak. Die entstof adjuvans Aluin aktiveer die sitosoliese NALP3/inflammasoom wat lei tot proIL-1β-splyting in bioaktiewe IL-1β.

Tolagtige reseptore.

TLR'e is tipe I transmembraanproteïene met 'n ekstrasellulêre aminoterminus en 'n intrasellulêre karboksieterminus. Hulle is saamgestel uit verskeie domeine, insluitend ekstrasellulêre leusienryke herhaling (LRR) met een of twee sisteïenryke streke en 'n intrasellulêre tol/IL-1 reseptor (TIR) ​​domein, vernoem na sy homologie met die IL-1 reseptor. Mense druk 10 TLR's uit: a) oppervlakuitgedrukte TLR'e sluit TLR2 (bakteriële lipopeptiede), TLR4 (lipopolisakkaried) en TLR5 (flagellin) in b) endosomale TLR'e sluit TLR7 en 8 [enkelstrengs RNA (30,31)] en TLR9 (ongemetileerde CpG) in DNA). Betrokkenheid van TLR's aktiveer intrasellulêre seinkaskades via myeloïde differensiasiefaktor 88 (MyD88)-afhanklike en MyD88-onafhanklike weë (32), insluitend IL-1-reseptor-geassosieerde kinase-4 (IRAK-4) werwing, wat kulmineer in NF-KB aktivering en uitdrukking van pro-inflammatoriese sitokiene, soos TNF , IL-6 en pro-IL1β [let daarop dat verwerking na volwasse IL-1β Nacht-domein leusienryke herhaling en piriendomein (PYD)-bevattende proteïen 3 (NALP3) inflammasoom (INFL) aksie vereis]. TLR-stimulasie kan ook lei tot die aktivering van verskeie ander intrasellulêre seinweë soos dié wat Jun N-terminale kinase, mitogeen-geaktiveerde proteïenkinase (33,34), interferon-regulerende faktor (IRF's) en die FAS-geassosieerde doodsdomein-geïnduseerde betrek apoptose pad (32).

Die belangrikheid van die TLR-weg vir gasheerverdediging by pasgeborenes en babas is duidelik in die kliniese gevolge van TLR-wegdefekte. Defekte van seinmolekules stroomaf van TLR'e, insluitend IRAK4- en MyD88-tekort lei tot selektiewe vatbaarheid vir piogeniese infeksies (dikwels streptokokke en stafilokokke) tydens die kinderjare met verbetering later in die lewe (35-37).

Naelstringbloedmonosiete van voltermyn menslike pasgeborenes druk normale hoeveelhede TLR'e uit, maar op TLR-gemedieerde stimulasie in heel naelstrengbloed (m.a.w., 100% vol/vol outoloog, adenosienryke plasma), agoniste van TLRs 1-7 demonstreer 'n 1-3 log inkorting in TNF-α produksie relatief tot volwasse perifere bloed monosiete (15). Een van die meganismes wat vir hierdie inkorting verantwoordelik is, is dat tydens die hipoksie en stres wat met die geboorteproses gepaardgaan, plasmakonsentrasies van adenosien, 'n endogene immuunonderdrukkende purienmetaboliet, toeneem. Adenosien kan werk via A3 adenosienreseptore op neonatale mononukleêre selle om produksie van cAMP te veroorsaak, 'n belangrike tweede boodskapper wat TLR-gemedieerde produksie van Th1-polariserende sitokiene inhibeer (4,9). Ander studies het getoon dat LPS-geïnduseerde response van pasgebore mononukleêre selle by geboorte verminder word as gevolg van verminderde uitdrukking van die TLR-adaptermolekule MyD88 (38) en deur mislukking van nukleosoomhermodellering by die IL-12-promotor (39). Verswakte TLR agonis-geïnduseerde produksie van tipe I IFN's van menslike neonatale plasmasitoïed DC's (pDC's) en neonatale monosiet-afgeleide DC's (moDC) is ook beskryf (40,41).

In teenstelling met agoniste van TLRs 1-7, is TLR8 agoniste, insluitend TLR7/8 agoniste, in staat om robuuste immuunresponse te veroorsaak deur menslike neonatale APC, vergelykbaar met dié van gesonde volwasse kontroles (42). Blootstelling van menslike neonatale koordbloed-afgeleide monosiete en APC's, insluitend myeloïede dendritiese selle en moDC's, aan TLR8-agoniste veroorsaak robuuste (m.a.w., volwasse vlak) fosforilering van p38 MAP-kinase, NF-KB-aktivering, pro-inflammatoriese sitokienproduksie (TNF, IL-12), en opregulering van ko-stimulerende molekules (bv., CD40).

Retinoïensuur-induseerbare geen-agtige reseptore.

Tydens die infeksiesiklus van sommige virusse word dubbelstring-RNA geproduseer wat in die sel-sitosol opgespoor kan word deur retinoïensuur-induseerbare geenagtige reseptore (RLR's), soos retinoïensuur-induseerbare geen I (RIG-I) en melanoomdifferensiasie-geassosieerde geen 5 (MDA-5). Hierdie sitoplasmiese proteïene is saamgestel uit aminoterminale kaspase-werwingsdomeine (CARDs) en 'n karboksieterminale helikasedomein (43,44). RLR-aktivering veroorsaak CARD-domeininteraksie met die CARD-domein-bevattende adapterproteïen, IFN-β-promotor-stimulator (IPS)-1 (ook bekend as mitochondriale antivirale seinproteïen, virus-geïnduseerde seinadapter, en CARD-adapter wat IFN-β induseer) na IRF3 en NF-KB aktivering. Min is bekend oor die ontwikkelingsuitdrukking van RLRs by geboorte en in die neonaat, 'n belangrike area van toekomstige studie.

Nukleotied-oligomerisasie-domeinagtige reseptore.

Nukleotied-oligomerisasie-domein-agtige reseptore (NLR's) bespeur bakteriële komponente en sluit lede van die nukleotied-bindende oligomeriseringsdomein (NOD) subfamilie en NLR's in wat met die INFL geassosieer word. Die NOD-proteïene in mense is 'n familie van >20 sitosoliese proteïene. Struktureel is hulle saamgestel uit: a) 'n veranderlike N-terminale effektor-bindende domein, gewoonlik bestaande uit 'n PYD of CARD, wat in staat is om homotipiese en heterotipiese binding te reguleer b) 'n sentraal geleë NOD-domein en c) 'n C-terminale ligand-herkenning domein, wat uit LRR'e saamgestel kan word. Soos met die RLR's, is min bekend oor die ontwikkelingsuitdrukking van NOD's by geboorte en in die neonaat.

Die INFL is 'n sitosoliese multikomponent proteïenkompleks, insluitend caspase-1, wat by aktivering pro-IL-1β tot die kragtige pro-inflammatoriese sitokien IL-1β klief. IL-1β speel 'n sentrale rol in die aanvang van bevalling, veral in die konteks van intrauteriene infeksie/ontsteking. 'n Onlangse studie het bevind dat: a) kaspase-1-konsentrasie in die vrugwater toeneem as 'n funksie van swangerskap-ouderdom b) vroue met spontane termynbevalling 'n hoër mediaan kaspase-1 vrugwaterkonsentrasie gehad het as vroue met termyn sonder bevalling, wat daarop dui dat die INFL kan geaktiveer word in spontane bevalling op termyn en c) hoër kaspase-1 vlakke was geassosieer met infeksie/inflammasie (45). Menslike neonatale monosiete, veral dié van premature pasgeborenes, toon verswakte IL1-β-produksie na LPS (45a) en tot lipoteichoïese sure (45b). 'n Soektog van Pubmed het geen publikasies opgelewer wat verband hou met INFL-funksie by geboorte nie.

C-tipe lektienreseptore.

C-tipe lektienreseptore (CLR's) kan geproduseer word as afgeskeide oplosbare proteïene, insluitend mannosebindende lektien (MBL), long-oppervlakaktiewe proteïen A, of as transmembraanproteïene soos selektiene, mannosereseptor en die DC-spesifieke ICAM-3-grypende nie-intregrien (DC-TEKEN). MBL is 'n akute fase plasma proteïen waarvan die uitdrukking in die lewer opgereguleer word tydens inflammasie. MBL herken 'n verskeidenheid koolhidraatpatrone wat op aansteeklike mikroörganismes voorkom, insluitend bakterieë (bv., Staphylococcus aureus), swamme (bv., Saccharomyces cerevisiae), en virusse (bv., MIV) en op veranderde selfglikoproteïene (bv., afwykende glikosilering van kankerselle). MBL-binding aan koolhidraatteikens veroorsaak aktivering van MBL-geassosieerde serienprotease, splitsing van komplementproteïene en bevorder opsonisering/membraanaanvalkompleksvorming (46). MBL kan ook direk as 'n opsonien optree deur aan reseptore te bind, wat fagositose bevorder (46) en sitokienproduksie kan moduleer in vitro en in vivo (47) speel daardeur belangrike rolle in neonatale infeksie. Plasma MBL-konsentrasies in beide premature en voltermyn neonate is laer as dié van volwassenes (48), maar neem geleidelik toe gedurende die eerste weke van die lewe, moontlik as gevolg van die skewe neonatale sitokienreaksies na IL-6, wat die akute fase reaksie (3,4). MBL-tekort word geassosieer met 'n verhoogde risiko van bakteriële sepsis (49).

Uit die oogpunt van aangebore immuunmodulasie van entstofreaksies, verhoog MBL-tekort muis Ag-spesifieke IgG-produksie na immunisering met tetanustoksoïed-gekonjugeerde groep B Streptokokke polisakkariedentstof of tetanustoksoïed alleen (50). Hierdie data dui daarop dat MBL onder sekere omstandighede Ab-produksie kan inhibeer. Verdere karakterisering van die MBL-weg kan die ontwerp van entstowwe verskaf wat sulke inhiberende MBL-effekte minimaliseer.

Ontwikkelingsuitdrukking van antimikrobiese proteïene en peptiede.

APP's wat deur leukosiete en epiteelselle uitgedruk word, is antieke komponente van aangebore immuunverdediging wat veral bekend is vir hul vermoë om mikroörganismes dood te maak en hul oppervlakkomponente te neutraliseer. Sommige APP's toon egter ook aktiwiteit in die modulering van aanpasbare immuunresponse. Daar is byvoorbeeld onlangs getoon dat bakteriedodende/deurlaatbaarheid-verhogende proteïen (BPI), 'n neutrofiel-afgeleide primêre korrelproteïen met endotoksienbindingsaktiwiteit, APC-funksie verbeter (50a). Neonate het 'n tekort aan BPI-uitdrukking, wat die moontlikheid verhoog wat ook die lewering van natuurlik afgestorte Gram-negatiewe bakteriële LPS-buitemembraanblare aan APC's kan benadeel. Defensienpeptiede kan die produksie van antivirale IFN'e verbeter, wat belangrik is vir Th1-polarisasie en kruisaanbieding (51). Katelisidienpeptiede, wat in neutrofiel sekondêre korrels voorkom, verbeter aanpasbare immuunresponse in vivo. Inderdaad is daar 'n ouderdom-afhanklike rypwording in die uitdrukking in menslike neonatale bloedplasma van 'n wye reeks APPs, en dus tot die mate wat hierdie molekules bydra tot die modulering van adaptiewe immuunresponse, kan tekortkominge in hul uitdrukking bydra tot verswakte adaptiewe response.

Die onlangse vordering met die definisie van PRR's en APP's wat betrokke is by die verwekking van aangebore immuunresponse en daardeur modulering van aanpasbare immuniteit bied nuwe geleenthede om daardie funksie van byvoegmiddels in tans toegediende entstowwe te verstaan, soos hieronder uiteengesit.

Betrokkenheid van aangebore immuniteit deur tans goedgekeurde neonatale en baba-entstowwe

Dit word toenemend besef dat 'n belangrike determinant van entstofdoeltreffendheid die vermoë van 'n gegewe entstof is om die aangebore immuunstelsel te aktiveer om APC-funksie en Th1-polariserende adaptiewe response te verbeter (52). Tans is die twee entstowwe wat gereeld by geboorte by mense gegee word, die Bacillus Calmette-Guerin (BCG) entstof en die hepatitis B (HepB) entstof (Tabel 1). BCG is in staat om 'n sterk Th1-tipe immuunrespons in menslike neonatale selle te veroorsaak in vitro (53) en in vivo (54), wat deels te danke is aan sy vermoë om verskeie TLR's uitgedruk deur APC's te aktiveer (55). Die BCG-entstof demonstreer dat die menslike neonatale immuunstelsel onder sekere toestande in staat is om 'n beskermende Th1-tipe reaksie op te stel (56), maar die onderliggende meganismes van die doeltreffendheid daarvan by geboorte word nie ten volle verstaan ​​nie. Onlangse werk het aangedui dat dit baie waarskynlik is dat aktivering van veelvuldige PRR's deur BCG 'n belangrike rol speel in die doeltreffendheid daarvan. Die BCG-entstof is 'n lewende bakterie en in staat om TLR2 (57,58) en TLR4 (57,58) te aktiveer op grond van sy selwand wat bestaan ​​uit peptidoglikaan, arabinogalaktaan en mikoliessure (59), en TLR9 deur sy CpG- ryk DNA (60). Meer onlangs is die moontlikheid dat BCG ook TLR8 betrek ook geopper op grond van assosiasies van TLR8 polimorfismes met vatbaarheid vir pulmonale tuberkulose, verhoogde vatbaarheid by mans (TLR8 is gekodeer op die X-chromosoom), en die vermoë van BCG om makrofaag TLR8 uitdrukking te veroorsaak (61).

Hepatitis B-virus (HBV) is 'n wêreldwye bedreiging vir openbare gesondheid wat >350 miljoen mense wêreldwyd chronies besmet het (62). Die HepB-entstof is saamgestel uit 'n virusagtige deeltjie wat die virale omhulselproteïen hepatitis B-oppervlak Ag (HBsAg) bevat, voorberei met behulp van rekombinante DNA-tegnologie. HepB-entstof is saamgestel uit 'n aluminiumbevattende hulpstof, maar is steeds onvolledig immunogenies aangesien ~ 10% van ingeënte populasies nie daarin slaag om immuunresponse teen HBsAg na immunisering op te stel nie (Tabel 1).

Haemophilus influenzae tipe b (Hib) gekonjugeerde entstowwe word aanvanklik op 6-8 weke ouderdom toegedien. Hib aktiveer getransfekteerde HEK293-selle op 'n TLR2-afhanklike en TLR4-afhanklike wyse, wat waarskynlik uitdrukking van bakteriële lipopeptiede (TLR2) en lipopolisakkaried (TLR4) (63,64) weerspieël (Tabel 1). Inderdaad, die buitenste membraanproteïenkompleks (OMPC) wat binne die Hib-OMPC-glikokonjugaat-entstof gevind word, is TLR2- en MyD88-afhanklik, en in die afwesigheid van TLR2 is die immunogenisiteit van die Hib-OMPC-entstof aansienlik verminder (64).

Benewens TLR-geïnduseerde entstofreaksies (65), is aktivering van RLRs [RIG-I en MDA-5 (66)] aangemeld vir die wilde-tipe maselsvirus, wat daarop dui dat die verswakte stamme wat vir inenting gebruik word, ook hierdie aangebore immuunweg (Tabel 1).

Tot op hede het die Amerikaanse voedsel- en dwelmadministrasie (FDA) 'n beperkte aantal menslike entstofhulpmiddels goedgekeur, waarvan die belangrikste aluminiumhidroksied, aluminiumfosfaat (gewoonlik na verwys as "Aluin") is. Aluin is 'n algemeen gebruikte adjuvans wat wêreldwyd in menslike en dier-entstowwe voorkom (HepB, DTaP, Hib, PCV7 en HepA Tabel 1) en is bekend vir sy vermoë om beskermende Th2-tipe reaksies te veroorsaak. Dit is onlangs gedemonstreer dat die sleutel tot Aluin se adjuvansaktiwiteit sy vermoë is om die NALP3/INFL (67,68) te aktiveer (Fig. 1). Hierdie gevolgtrekkings is gebaseer op die waarnemings dat IL-1β en IL-18 produksie deur makrofage in reaksie op Aluin in vitro vereis ongeskonde INFL sein. Boonop kon muise met 'n tekort aan NALP3, apoptose-geassosieerde spikkelsagtige proteïen wat 'n KAART of kaspase-1 bevat, nie 'n beduidende Ab-reaksie op 'n Ag toegedien met Aluin oplewer nie, terwyl die reaksie op volledige Freund se adjuvans ongeskonde gebly het. These data highlight the crucial role of the NALP3/INFL in Alum's adjuvant activity.

MF59 is an oil-in-water squalene emulsion and the precise mechanism of its adjuvant effects is still largely unknown (69). Recent studies have revealed that MF59 is a very efficient adjuvant due to its ability to activate and sustain tissue-resident DCs (69a). Studies using fluorescently labeled MF59 injected intramuscularly then observed 2 d later indicated partial localization in T cell areas of the draining lymph node (70). MF59 has also been documented to induce a significant influx of macrophages to the site of infection in mice, which is chemokine receptor 2 dependant (71). Of interest, the oil emulsion incomplete Freund's adjuvant (not licensed in humans due to its toxicity) induces optimal IgG1 and IgG2c in a NOD2-dependant manner (72).

Translational Research Toward Improved Adjuvants for Newborns and Infants

Given that newborns and young infants are susceptible to multiple bacterial and viral pathogens, neonatal immunization is of particular importance because: a) birth represents a likely point of contact of the newborn with healthcare providers, b) early life immunization is associated with a substantially higher rate of vaccination coverage than immunization given at later time points (2,73), c) vaccines that require multiple dosing regimens throughout infancy increase cost and reduce compliance, and (d) strategies involving immunization of the mother pose substantial logistical and medico-legal challenges. There is, therefore, an unmet medical need to develop vaccines that would be more effective very early in life or that would require fewer doses to generate durable and protective immune responses.

A novel approach to neonatal vaccination has recently been described, which uses an attenuated strain of the intracellular pathogenic bacterium Listeria monocytogenes to deliver Ag to the cytoplasm of APC (74). Vaccinated neonatal mice induced strong CD8 + and CD4 + T cell responses and were protected after wild-type challenge. Of note, L. monocytogenes is able to activate several PRRs including multiple NODs (IPAF, NALP3) (75) and can induce the expression of RIG-I (76), possibly accounting for its immunostimulatory properties. Therefore, this approach could potentially overcome preexisting hurdles of maternal immune response interfering with neonatal vaccine responses (77). This live attenuated vaccine seemed safe in this murine model in that there was no associated mortality and no bacteria were recovered from the spleens or liver of immunized newborn mice 7 d postvaccination.

Among the TLR agonists, TLR7/8 agonists hold particular promise as potential adjuvants for use in neonatal and infant vaccines as they induce robust production of the Th1-polarizing cytokines TNFα and IL-12 from neonatal (and adult) APCs that substantially exceeds responses induced by agonists of TLR-2, TLR-4, or TLR-7 (alone) (42,78). Therefore, TLR7/8 agonists have potential as novel neonatal vaccine adjuvants, due to their ability to activate both TLR-dependant and independent pathways (NALP3/INFL) mediating Th1-type responses from APC (78). In addition, human Treg express TLR8 and mediate reversal of Treg function on exposure to TLR8 agonists (79) (Fig. 2). Indeed TLR7/8 agonists, such as the synthetic low-molecular weight (<400 Da) antiviral imidazoquinoline compounds imiquimod and resiquimod (R848), have already been used as immunomodulators for many years against specific viral infections. The US FDA approved imiquimod for the treatment of external genital and perianal warts caused by certain strains of human papilloma virus (80), and it may also have activity against molluscum contagiosum (mulluscipox virus) (81–83). One of the main cellular targets of imiquimod is pDCs (IFN-α producing cells), which express high amounts of TLR7, whose engagement induced IFN-α in a MyD88-dependent manner (80,84).

TLR8 agonists activate human APCs and reverse human Treg function. TLR8 agonists, such as R848, ssRNA and stabilized immune modulatory RNA (SIMRA) strongly activate human APCs via TLR8-dependent and TLR8-independent mechanisms including activation of the NALP3 inflammasome inducing IL-1β production. Exposure of human neonatal APCs to TLR8 agonists induces robust phosphorylation of p38 MAP kinase and profound/prolonged disappearance of IkB-κ, resulting in robust induction of protective Th1-type immune responses, including production of IL-12 and up-regulation of the costimulatory molecule CD40. TLR8 agonists also reverse suppression mediated by human Treg cells, via both direct action on Treg as well as by induction of APC production of IL-6, a cytokine that renders Tresponder cells refractory to Treg-mediated inhibition.

R848 is an effective adjuvant for HBsAg vaccination in mice, increasing humoral and cellular immune responses. R848 used in combination with the TLR9 agonists CpG ODN further strengthened the immune response and long-lasting HBsAg-specific T cells displaying effector memory phenotype were detected in mice (85). R848 or topical application of imiquimod administered with Leishmania Ag induced protective Th1 immune responses in mice, compared with Leishmania Ag alone. In addition, s.c. vaccination also induced protective immunity whereas intramuscular vaccination did not (86). Indeed, conjugation of the TLR7/8 agonist to the HIV Gag protein improved the magnitude of Th1 and CD8 responses in adult Rhesus macaques (87). A combined TLR7/8 agonist compared with a pure TLR8 agonist can also induce greater Th1 responses and IFNα production from pDCs, which express TLR7 but not TLR8. IFNα is a key cytokine within a vaccine adjuvant setting, inducing Th1 differentiation (80,88), induction of cytotoxic T lymphocytes, enhancement of cross presentation and of primary Ab responses and DC activation (89). Novel TLR7 and TLR8 agonists referred to as stabilized immune modulatory RNA (SIMRA) compounds have recently developed and have distinct pharmacodynamic characteristics (90). SIMRA compounds demonstrate greater stability in human sera compared with linear RNA, which is rapidly degraded by ubiquitous RNases. In addition, SIMRA compounds and are able to activate TLR7 or TLR8 in HEK293 cells without the need for lipid carriers.

TLR9 agonists are also undergoing biopharmaceutical development for multiple indications, including as vaccine adjuvants for HBV by linking an immunostimulatory DNA sequence to the recombinant HBsAg. This vaccine formulation, which has currently completed phase III trials, may help drive Th1-type responses and reduce Th2 responses (91).

A murine study demonstrated that although the IPS-1 signaling pathway seems to be important for initial type I IFN responses, the TLR7/MyD88 pathway is needed for induction of protective immune responses to influenza A infection. Inactivated influenza virus vaccine failed to confer protection against lethal challenge with live influenza virus in TLR7-deficient and MyD88-deficient mice. Thus, protective adaptive immune responses to live attenuated influenza A virus strains are likely dependent on the TLR7-MyD88 pathway (92).


  • Witseerkeel
  • Hepatitis A and hepatitis B
  • Haemophilus influenzae type b (Hib) and influenza (flu)
  • Menslike papillomavirus (HPV)
  • Measles and mumps
  • Meningococcus
  • Pertussis (whooping cough)
  • Pneumococcal disease, such as pneumonia
  • Polio
  • Rotavirus
  • Rubella
  • Tetanus
  • Tuberculosis (TB)
  • Varicella (chickenpox)
  • You will get a Vaccine Information Statement (VIS) for each vaccine your child receives. The VIS will explain what the vaccine is for and its risks and benefits. You may be able to read the VIS before your child receives the vaccine. The VIS may be printed or delivered electronically to you.
  • Vaccines are given on a recommended schedule. Your child may need some vaccines each year to protect him or her from new forms of a virus, such as the flu. He or she will receive several vaccines, starting a few weeks after birth. He or she will need 2 or more doses of each vaccine. Some of the vaccines are combined. He or she may also need boosters. Follow the immunization schedule your child's healthcare provider gives you, or bring your child in for catch-up doses.
  • Some vaccines will protect your child when he or she is older. For example, hepatitis A is not usually a risk for children. Immunization will help protect your child from it when he or she is an adult.
  • Some vaccines are only given for certain situations. Your child may need rabies vaccines if he or she is bitten by an animal that can carry rabies. He or she may need certain vaccines if he or she is traveling to another country. Tell his or her healthcare provider as far as possible before your child travels. The vaccines may take several weeks to become effective.
  • Vaccines will not increase your child's risk for autism. Some parents worry that vaccines increase the risk for autism. Research shows there is no connection between vaccines and autism. Talk to your child's healthcare provider if you have concerns about the risk for autism.
  • Keep a record of the vaccines your child receives. Your healthcare provider may also keep electronic records. Records will help you make sure your child receives all the vaccines he or she needs, and at the right times. He or she may need the records to be able to enroll in school or college, or to play sports. Bring the record with you to each immunization visit.

The risks and benefits of vaccination.

Nobody likes getting shots, but at the end of the day vaccines and shots save lives. The diseases that vaccines prevent can be deadly, and these shots work with the body’s natural defense to develop immunity to these deadly diseases.

When bacteria or viruses invade your body, they attack and multiply. This is called an infection, and it’s what causes illnesses. Our immune system then fights this infection, and has a supply of cells or antibodies that remember the infection and can fight that disease in the future.

The vaccines we get can help our bodies develop immunity, as tiny doses of the disease are introduced to our body, without causing illness. It helps the immune system develop the same response as a real infection, so you can develop antibodies and fight it in the future.

Some people argue that natural immunity is best for your body. While this is true, many immune systems can't handle the virus that comes, and things like measles, polio, and smallpox can kill children or leave devastating results like paralysis or neurological damage. Immunizations are a much safer way to help immune systems create the antibodies needed to fight these diseases.

Registered nurses or other educated healthcare professionals ones who administer vaccines. These nurses are trained in school about the proper ways to administer vaccines, what reactions to watch out for, and can explain vaccine safety to help ensure you are educated and comfortable.

As more health professionals enter the field, there are more trained experts to help with vaccine safety.

Risks of vaccination.

There are some very rare and very mild side effects that can be the result of vaccinations. These side effects completely depend on the immunization you got, and how your specific body will react to it. While there are side effects, as with any medication, it’s important to note that unvaccinated children run the risk of spreading diseases or catching a deadly disease themselves.

Mild side effects.

There are sometimes very mild side effects from getting a vaccine. As the vaccine enters your body and is pretending to be the infection, you may get some of the symptoms of that disease like a cold symptoms, or a slight fever that shows your body is fighting the infection. There may be soreness of muscles or redness at the injection site. All of these very mild side effects go away in a couple of days.

Rare side effects.

There is a very rare chance you or your child could have more severe side effects that come from vaccines. High fevers, rashes, or neurological episodes are these very rare side effects. Medical professionals are trained to deal directly with these kinds of side effects, and each of them is extremely rare—more rare than getting the disease that is being immunized against.

Allergieë.

Rarely, individuals will be allergic to vaccinations and can have reactions to their shots. While allergic reactions can be very dangerous, again, they are extremely rare. The CDC reports that in 2015, only 33 people had a serious allergic reaction out of 25 million vaccines given. Many people have genetic indications that they could be allergic to vaccines and are able to work with health professionals to stay safe.

Benefits of vaccinations.

Disease control.

Vaccines are extremely effective at controlling or eliminating dangerous diseases. The World Health Organization reports that the measles vaccine has prevented more than 20 million deaths since 2000.

Smallpox has been completely eradicated thanks to vaccinations, and polio is not far behind. Polio vaccines are still given to help keep control of the disease until it has been globally removed.

Immunizations have a direct impact on disease and virus control in the United States, and across the globe. Immunizations have turned deadly, devastating diseases into preventable diseases that are no longer life-threatening.

Herd immunity.

When more people have vaccinations, it makes everyone less likely to get the disease that is vaccinated against. This control of diseases is called herd immunity, and benefits the entire community.

For example, routine measles vaccines are high in the United States, with 91% of preschool children vaccinated. Measles has an extremely low occurrence rate as a result. But as specific areas dip in the number of vaccines, outbreaks have been seen. In 2018, 17 measles outbreaks impacting more than 370 people were confirmed. This is a direct result of localized areas opting out of vaccines.

When more people decide not to vaccinate, the diseases they prevent against have the potential to flare up or even get out of control. This is why research on vaccine safety is crucial health professionals want to explain the slight risks of vaccines, and share how the benefits outweigh any risk because of things like herd immunity, that keep everyone safe.

Vaccines have been a hot topic for debate as research has come out about them. Many controversial studies, like the research about vaccines causing autism, have since been discredited. It’s important to look to health professionals as you research and learn about vaccinations and how they can benefit your family.


Your Child's Immunizations

Babies are born with protection against some diseases because their mothers pass antibodies (proteins made by the body to fight disease) to them before birth. Breastfed babies continue to get more antibodies in breast milk. But in both cases, the protection is temporary.

Immunization (vaccination) is a way to create immunity to (protection from) some diseases. This is done by using small amounts of a killed or weakened germ that causes the disease.

Germs can be viruses (such as the measles virus) or bacteria (such as pneumococcus). Vaccines stimulate the immune system to react as if there were a real infection. It fends off the "infection" and remembers the germ. Then, it can fight the germ if it enters the body later.

What Are the Types of Vaccines?

There are a few different types of vaccines. Dit sluit in:

  • Verswak(weakened) live viruses are used in some vaccines such as in the measles, mumps, and rubella (MMR) vaccine.
  • Killed(inactivated) viruses or bacteria are used in some vaccines, such as in IPV.
  • Toxoid vaccines contain an inactivated toxin produced by the bacterium. For example, the diphtheria and tetanus vaccines are toxoid vaccines.
  • Conjugate vaccines (such as Hib) contain parts of bacteria combined with proteins.

The American Academy of Pediatrics (AAP) recommends that kids get combination vaccines (rather than single vaccines) whenever possible. Many vaccines are offered in combination to help reduce the number of shots a child receives.

What Vaccines Do Kids Need?

The following vaccinations and schedules are recommended by the AAP. Some variations are normal, and recommendations change as new vaccines are developed. Your doctor will talk to you about the right vaccinations and schedule for your child.

Vaccine Concerns

Some parents may hesitate to have their kids vaccinated. They have questions or worry that a child might have a serious reaction or get the illness the vaccine prevents. But the components of vaccines are weakened or killed. In some cases, only parts of the germ are used. So they're unlikely to cause any serious illness.

Some vaccines may cause mild reactions, such as soreness where the shot was given or a fever. But serious reactions are rare. The risks of vaccinations are small compared with the health risks of the diseases they're intended to prevent.

Immunizations are one of the best means of protection against contagious diseases.


Formaldehyde content of vaccines licensed for use in the United States

Td (adult)/ DT

Quantity per dose: ≤ 0.005 mg – 0.1 mg

DTaP (Daptacel®, Infanrix®)

Quantity per dose: ≤ 0.005 mg – ≤ 0.1 mg

DTaP-Hep B IPV (Pediarix®)

DTaP-IPV (Kinrix®, Quadracel®)

DTaP-IPV-Hib (Pentacel®)

Quantity per dose: < 0.005 mg

Hepatitis A (Havrix®, Vaqta®)

Hepatitis A - Hepatitis B (Twinrix®)

Hib (ActHIB®, HIBERIX®)

Quantity per dose: < 0.005 mg

Hepatitis B (RECOMBIVAX®)

Quantity per dose: < 0.0075 mg (pediatric) < 0.015 mg (adult and dialysis formulations)

Meningococcal vaccines

Polio (IPOL®)

Japanese encephalitis vaccine (IXIARO®)

Quantity per dose: < 200 ppm

Tdap (ADACEL®, Boostrix®)

Griep

Not all influenza vaccines contain formaldehyde, but some preparations contain amounts between < 0.005 – 0.1 mg.


Pediatric Infectious Disease Expert Guidance: Should My Child Get the COVID-19 Vaccine?

Vaccination is one way we can help get kids back to in-person activities.

The Food and Drug Administration expanded emergency use authorization of the Pfizer-BioNTech COVID-19 vaccine to include adolescents 12 to 15 years of age on May 10, 2021. The Centers for Disease Control and Prevention followed with recommendations endorsing use in this age group after their advisory group meeting on May 12. The American Academy of Pediatrics also supports this decision.

Dr. Debbie-Ann Shirley is an associate professor of pediatrics at the University of Virginia specializing in pediatric infectious diseases. Here she addresses some of the concerns parents may have about their teen or preteen getting the COVID-19 vaccine.

1. Does the vaccine work in adolescents?

Yes, recently released data from Pfizer-BioNTech shows that the COVID-19 vaccine seems to work really well in this age group. The COVID-19 vaccine was found to be 100% efficacious in preventing symptomatic COVID-19 in an ongoing clinical trial of children in the U.S. aged 12 to 15. Adolescents made high levels of antibody in response to the vaccine, and their immune response was just as strong as what has been seen in older teens and young adults 16-25 years of age.

2. How do I know whether the vaccine is safe for my child?

So far, the COVID-19 vaccine appears to be safe and well tolerated in adolescents. All of the COVID-19 vaccines authorized for use in the U.S. have undergone rigorous study, but we don’t want to assume that children are little adults. This is why it is so important to study these vaccines just as carefully in children before health authorities could recommend use. Ongoing studies will continue to follow vaccinated children closely and robust safety monitoring will help rapidly identify rare or unexpected concerns if they emerge.

The Pfizer-BioNTech COVID-19 vaccine was found to be 100% efficacious in preventing symptomatic COVID-19 in children ages 12 to 15 years.

3. I thought children were low-risk – do they still need to get the vaccine?

Currently, children represent nearly one-quarter of all new reported weekly COVID-19 cases in the U.S. While serious illness from COVID-19 is rare in children, it does occur – thousands of children have been hospitalized and at least 351 children have died from COVID-19 in the U.S. Some children who get seriously ill from COVID-19 may have underlying health conditions, but not all do. Vaccination will help protect children from developing serious illness.

Additionally, since adolescents can transmit COVID-19 to others, vaccinating children may prove to be an important part of safely getting back to normal activities of life, including attending school in person, participating in team sports and spending time with friends. A large survey of school-aged children showed that children in full or partial virtual school reported lower levels of physical activity, less in-person time socializing with friends and worse mental or emotional health compared with those receiving full in-person schooling. Children are experiencing unprecedented increases in indirect adverse health and educational consequences related to the pandemic, and we need to find ways to help them get quickly and safely back to normal life. Vaccination is one of them.

4. What side effects might I expect for my child?

Nonsevere side effects may be experienced following vaccination. The most commonly reported side effects have been pain and swelling at the injection site. Other common side effects include tiredness and headache. Similar to young adults, some adolescents have experienced fever, chills, muscle aches and joint pain, which may be more common after the second dose. These effects are short-lived, however, and most resolve within one to two days.

Some adolescents may faint when receiving an injection. If this is a concern for your child, let your vaccine administration site know ahead of time – your child can be given the vaccine while they’re seated or lying down to avoid injuries from falling.

Children represent nearly one-quarter of all new reported weekly COVID-19 cases in the U.S.

5. Have there been any severe reactions among children?

No serious adverse events related to vaccination were reported in the Pfizer-BioNTech clinical trial. Serious allergic reactions have rarely been reported in older people. Anyone with a known severe or immediate allergy to the vaccine or any component of the vaccine should not get the vaccine. If your child has a history of any severe allergic reactions or any type of immediate allergic reaction to a vaccine or injectable therapy, let the vaccine site administrator know so that your child can be monitored for at least 30 minutes after getting the vaccine.

Parents should talk to a trusted health care provider or allergist if they have specific questions about the possibility of an allergic reaction in their child.

6. When will a COVID-19 vaccine be authorized for children younger than 12 years?

COVID-19 vaccine makers have begun or are planning to begin testing COVID-19 vaccines in younger children. As more information becomes available, the authorized age recommendations may change. Children ages 2-11 years old could potentially be eligible as early as the end of this year.

7. If I’ve been vaccinated but my child hasn’t, could I still give the virus to them?

The COVID-19 vaccines do not contain live COVID-19 virus, so they cannot cause COVID-19. Rather, getting vaccinated will help protect both you and your children from COVID-19. Studies have shown that vaccinated pregnant and lactating mothers can pass protective immunity on to their young infants across the placenta and in breast milk – one more benefit of vaccination.

Though researchers are still learning how well the vaccine can help prevent spread, vaccination is still an important way to limit infecting people who are not yet eligible for the vaccine, like younger children.

Written by Debbie-Ann Shirley, Associate Professor of Pediatrics, University of Virginia.


Science as Process

You may think of science as a large and detailed body of knowledge, but science is actually more of a process than a set of facts. The real focus of science is the accumulation and revision of scientific knowledge. Science is a special way of gaining knowledge that relies on evidence and logic. Evidence is used to continuously test ideas. Through time, with repeated evidence gathering and testing, scientific knowledge advances.

We've been accumulating knowledge of vaccines for more than two centuries. The discovery of the first vaccine, as well as the process of vaccination, dates back to 1796. An English doctor named Edward Jenner observed that people who became infected with cowpox did not get sick from smallpox, a similar but much more virulent disease (Figure (PageIndex<2>)). Jenner decided to transmit cowpox to a young child to see if it would protect them from smallpox. He gave the child cowpox by scratching liquid from cowpox sores into the child's skin. Then, six weeks later, he scratched liquid from smallpox sores into the child's skin. As Jenner predicted, the child did not get sick from smallpox. Jenner had discovered the first vaccine, although additional testing was needed to show that it really was effective.

Figure (PageIndex<2>): A young child covered with skin lesions from smallpox. Until it was eradicated, this highly contagious infection caused many deaths, and those that survived were often severely scarred for life.

Almost a century passed before the next vaccine was discovered, a vaccine for cholera in 1879. Around the same time, French chemist Louis Pasteur found convincing evidence that many human diseases are caused by germs. This earned Pasteur the title of "father of germ theory." Since Pasteur's time, vaccines have been discovered for scores of additional diseases caused by "germs," and scientists are currently researching vaccines for many others.


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