期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 205, 期 7, 页码 1543-1550出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20080321
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资金
- Agence Nationale de la Recherche,
- Programme Hospitalier de Recherche Clinique
- European Union [LHSP-CT-2005-018736]
- BNP Paribas Foundation
- March of Dimes
- Dana Foundation
- Candi'Oser Association
- Fondation pour la Recherche Medicale
- Pierre et Marie Curie University
- Howard Hughes Medical Institute
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-12R beta 1- 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.
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