Utilize este identificador para referenciar este registo: http://hdl.handle.net/10400.16/900
Título: Mutations in STAT3 and IL12RB1 impair the development of human IL-17 – producing T cells
Autor: Beaucoudrey, L.
Puel, A.
Filipe-Santos, O.
Cobat, A.
Ghandil, P.
Chrabieh, M.
Feinberg, J.
Bernuth, H.
Samarina, A.
Jannière, L.
Fieschi, C.
Stéphan, J.
Boileau, C.
Lyonnet, S.
Jondeau, G.
Cormier-Daire, V.
Merrer, M.
Hoarau, C.
Lebranchu, Y.
Lortholary, O.
Chandesris, M.
Tron, F.
Gambineri, E.
Bianchi, L.
Rodriguez-Gallego, C.
Zitnik, S.
Vasconcelos, J.
Guedes, M.
Vitor, A.
Marodi, L.
Chapel, H.
Reid, B.
Roifman, C.
Nadal, D.
Reichenbach, J.
Caragol, I.
Garty, B.
Dogu, F.
Camcioglu, Y.
Gülle, S.
Sanal, O.
Fischer, A.
Abel, L.
Stockinger, B.
Picard, C.
Casanova, J.
Data: Jul-2008
Editora: Rockefeller University Press
Citação: J Exp Med. 2008 Jul 7;205(7):1543-50
Resumo: Abstract 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.
Peer review: yes
URI: http://hdl.handle.net/10400.16/900
ISSN: 0022-1007
Versão do Editor: www.jem.org/cgi/doi/10.1084/jem.20080321
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