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Nun estudo con ratos alérxicos aos [[cacahuete]]s, comprobouse que carecían de IL-12, o que suxire que a molécula detén normalmente as alerxias alimentarias. Estase agora a investigar se os resultados atopados en ratos son igual de intensos en humanos.<ref>{{cite journal |author=Temblay JN, Bertelli E, Arques JL, Regoli M, Nicoletti C |title=Production of IL-12 by Peyer patch-dendritic cells is critical for the resistance to food allergy |journal=J. Allergy Clin. Immunol. |volume=120 |issue=3 |pages=659–65 |date=September 2007 |pmid=17599398 |doi=10.1016/j.jaci.2007.04.044 |url=http://linkinghub.elsevier.com/retrieve/pii/S0091-6749(07)00942-6}}</ref><ref>{{cite news |title=Food allergy molecule discovered |newspaper=BBC News |date=1 July 2007 |url=http://news.bbc.co.uk/2/hi/health/6254576.stm}}</ref>
== A IL-12 ande as mutacións no receptor de IL-12 receptor β1 mutations ==
InterleukinA 12 (IL-12) isprodúcena producedas by[célula activatedpresentadora antigen-presentingde cellsantíxenos|células presentadoras de antíxeo]] activadas ([[dendriticcélula dendrítica|células cellsdendríticas]], [[macrophagesmacrófago]]s).<ref name="pmid10959079">{{cite journal | author = Dorman SE, Holland SM | title = Interferon-gamma and interleukin-12 pathway defects and human disease | journal = Cytokine Growth Factor Rev. | volume = 11 | issue = 4 | pages = 321–33 | year = 2000 | pmid = 10959079 | doi = 10.1016/s1359-6101(00)00010-1}}</ref> ItPromociona promoteso thedesenvolvemento developmentde ofrespostas [[célula Th1 cell|Th1]] responsese andé isun aindutor powerfulpoderoso inducerda ofprodución de [[IFNγ]] productionpolas bycélulas T ande [[NK cells]].<ref>{{Cite book | author = Newport MJ, Holland SM, Levin M, Casanova J-L | chapter = Inherited disorders of the interleukin-12/23-interferon gamma axis | editor = Ochs HD, Smith CI, Puck J | title = Primary immunodeficiency diseases : a molecular and genetic approach | date = 2007 | publisher = Oxford University Press | location = New York | isbn = 0-19-514774-X | pages = 390–401 }}</ref>
AAtopouse childnun withneno que tiña infeccións polo [[Bacillusbacilo de Calmette–Guérin]] ande ''[[Salmonella enteritidis]]'' infectionunha wasgran found to have a large[[deleción]] [[homozygoushomocigoto|homocigótica]] deletionno withinxene theda IL-12subunidade p40 subunitda geneIL-12, precludingque expressionimpedía ofa functionalexpresión da citocina IL-12 p70 cytokinefuncional bypolas activatedcélulas dendriticdendríticas cellsactivadas ande phagocytesos [[fagocito]]s. AsComo resultado, a result,produción de IFNγ productionpolos bylinfocitos the child'sdo lymphocytesrapaz wasestaba markedlymoi impairedalterado.<ref name="Altare_1998">{{cite journal | author = Altare F, Durandy A, Lammas D, Emile JF, Lamhamedi S, Le Deist F, Drysdale P, Jouanguy E, Döffinger R, Bernaudin F, Jeppsson O, Gollob JA, Meinl E, Segal AW, Fischer A, Kumararatne D, Casanova JL | title = Impairment of mycobacterial immunity in human interleukin-12 receptor deficiency | journal = Science | volume = 280 | issue = 5368 | pages = 1432–5 | year = 1998 | pmid = 9603732 | doi = 10.1126/science.280.5368.1432 }}</ref>
ThisIsto suggestedsuxire thatque a IL-12 isé essentialesencial forpara protectiveter immunityunha toinmunidade intracellularprotectora contra [[bacteria]]s intracelulares suchcomo as [[mycobacteriamicobacteria]]s ande ''[[Salmonella]]''.
Un apoio a esta idea foi a observación de que é importante un receptor para a IL-12 para a produción de IFNγ polos linfocitos. As células T e NK de sete pacientes non relacionados que padecían graves infeccións por micobacterias e ''Salmonella'' non podían producir IFNγ cando eran estimulados con IL-12.<ref name="Altare_1998"/> Con todo, os pacientes mantíñanse saudables. Descubriuse que tiñan [[mutación]]s na cadea β1 do receptor de IL-12, que dan lugar a [[codón de parada|codóns de parada]] prematuros no dominio extracelular, que orixinan a falta de resposta a esta citocina, o que de novo demostra o papel esencial da IL-12 na defensa do hóspede.
Support is lent to this idea by the observation that a [[receptor (biochemistry)|receptor]] for IL-12 is important for IFNγ production by lymphocytes. T and NK cells from seven unrelated patients who had severe idiopathic mycobacterial and Salmonella infections failed to produce IFNγ when stimulated with IL-12.<ref name="Altare_1998"/> The patients were otherwise healthy. They were found to have mutations in the IL-12 receptor β1 chain, resulting in premature stop codons in the extracellular domain, resulting in unresponsiveness to this cytokine, again demonstrating IL-12′s crucial role in host defense.
DefectiveAs respostas Th1 ande Th17 immuneinmunitarias responsesdefectivas leadingproducen tounha [[chroniccandidiase mucocutaneousmucocutánea candidiasiscrónica]] resultcomo fromresultado adunha mutationmutación furthermáis downstream''[[augas inabaixo]]'' the IL-12da [[signallingvía pathwayde sinalización]] de IL-12. Este Thetrazo traitxenético wasfoi mappedmapado toen mutationsmutacións inno thexene [[STAT1]] gene, whichque wereestaban associatedasociados withcunha lowerprodución productionmáis ofbaixa interferonde interferón-γ, [[IL-17]], ande [[IL-22]] inen responseresposta toa IL-12 orou IL-23 receptor associateda [[Jak2]] andasociado ao receptor de IL-23 e a actividade de [[tyrosinetirosina kinasequinase 2|Tyk2]] activity.<ref name="pmid21714643">{{cite journal | author = van de Veerdonk FL, Plantinga TS, Hoischen A, Smeekens SP, Joosten LA, Gilissen C, Arts P, Rosentul DC, Carmichael AJ, Smits-van der Graaf CA, Kullberg BJ, van der Meer JW, Lilic D, Veltman JA, Netea MG | title = STAT1 mutations in autosomal dominant chronic mucocutaneous candidiasis | journal = N. Engl. J. Med. | volume = 365 | issue = 1 | pages = 54–61 | year = 2011 | pmid = 21714643 | doi = 10.1056/NEJMoa1100102 }}</ref>
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