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Mutations in STAT3 and IL12RB1 impair the development of human IL-17 – producing T cells

2008-07Journal article Open access
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dc.contributor.authorBeaucoudrey, L.
dc.contributor.authorPuel, A.
dc.contributor.authorFilipe-Santos, O.
dc.contributor.authorCobat, A.
dc.contributor.authorGhandil, P.
dc.contributor.authorChrabieh, M.
dc.contributor.authorFeinberg, J.
dc.contributor.authorBernuth, H.
dc.contributor.authorSamarina, A.
dc.contributor.authorJannière, L.
dc.contributor.authorFieschi, C.
dc.contributor.authorStéphan, J.
dc.contributor.authorBoileau, C.
dc.contributor.authorLyonnet, S.
dc.contributor.authorJondeau, G.
dc.contributor.authorCormier-Daire, V.
dc.contributor.authorMerrer, M.
dc.contributor.authorHoarau, C.
dc.contributor.authorLebranchu, Y.
dc.contributor.authorLortholary, O.
dc.contributor.authorChandesris, M.
dc.contributor.authorTron, F.
dc.contributor.authorGambineri, E.
dc.contributor.authorBianchi, L.
dc.contributor.authorRodriguez-Gallego, C.
dc.contributor.authorZitnik, S.
dc.contributor.authorVasconcelos, J.
dc.contributor.authorGuedes, M.
dc.contributor.authorVitor, A.
dc.contributor.authorMarodi, L.
dc.contributor.authorChapel, H.
dc.contributor.authorReid, B.
dc.contributor.authorRoifman, C.
dc.contributor.authorNadal, D.
dc.contributor.authorReichenbach, J.
dc.contributor.authorCaragol, I.
dc.contributor.authorGarty, B.
dc.contributor.authorDogu, F.
dc.contributor.authorCamcioglu, Y.
dc.contributor.authorGülle, S.
dc.contributor.authorSanal, O.
dc.contributor.authorFischer, A.
dc.contributor.authorAbel, L.
dc.contributor.authorStockinger, B.
dc.contributor.authorPicard, C.
dc.contributor.authorCasanova, J.
dc.date.accessioned2012-03-26T11:17:28Z
dc.date.available2012-03-26T11:17:28Z
dc.date.issued2008-07
dc.description.abstractAbstract The cytokines controlling the development of human interleukin (IL) 17--producing T helper cells in vitro have been difficult to identify. We addressed the question of the development of human IL-17--producing T helper cells in vivo by quantifying the production and secretion of IL-17 by fresh T cells ex vivo, and by T cell blasts expanded in vitro from patients with particular genetic traits affecting transforming growth factor (TGF) beta, IL-1, IL-6, or IL-23 responses. Activating mutations in TGFB1, TGFBR1, and TGFBR2 (Camurati-Engelmann disease and Marfan-like syndromes) and loss-of-function mutations in IRAK4 and MYD88 (Mendelian predisposition to pyogenic bacterial infections) had no detectable impact. In contrast, dominant-negative mutations in STAT3 (autosomal-dominant hyperimmunoglobulin E syndrome) and, to a lesser extent, null mutations in IL12B and IL12RB1 (Mendelian susceptibility to mycobacterial diseases) impaired the development of IL-17--producing T cells. These data suggest that IL-12Rbeta1- and STAT-3--dependent signals play a key role in the differentiation and/or expansion of human IL-17-producing T cell populations in vivo.por
dc.description.sponsorshipThe Laboratory of Human Genetics of Infectious Diseases is supported by the Agence Nationale de la Recherche, the Programme Hospitalier de Recherche Clinique, the European Union (grant LHSP-CT-2005-018736), the BNP Paribas Foundation, the March of Dimes, the Dana Foundation, and the Candi’Oser Association. L. de Beaucoudrey is supported by the Fondation pour la Recherche Medicale as part of the PhD program of Pierre et Marie Curie University. J.L. Casanova is an International Scholar of the Howard Hughes Medical Institute.por
dc.identifier.citationJ Exp Med. 2008 Jul 7;205(7):1543-50por
dc.identifier.issn0022-1007
dc.identifier.urihttp://hdl.handle.net/10400.16/900
dc.language.isoengpor
dc.peerreviewedyespor
dc.publisherRockefeller University Presspor
dc.relation.publisherversionwww.jem.org/cgi/doi/10.1084/jem.20080321por
dc.titleMutations in STAT3 and IL12RB1 impair the development of human IL-17 – producing T cellspor
dc.typejournal article
dspace.entity.typePublication
oaire.citation.conferencePlaceUnited States of Americapor
oaire.citation.endPage1550por
oaire.citation.issue205(7)por
oaire.citation.startPage1543por
oaire.citation.titleThe Journal of experimental medicinepor
rcaap.rightsopenAccesspor
rcaap.typearticlepor

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