Zheng, W. & Flavell, R.A. The transcription factor GATA-3 is necessary and sufficient for Th2 cytokine gene expression in CD4 T cells. Cell89, 587–596 (1997). ArticleCASPubMed Google Scholar
Mosmann, T.R. & Coffman, R.L. TH1 and TH2 cells: different patterns of lymphokine secretion lead to different functional properties. Annu. Rev. Immunol.7, 145–173 (1989). ArticleCASPubMed Google Scholar
Kuchroo, V.K. et al. T cell response in experimental autoimmune encephalomyelitis (EAE): role of self and cross-reactive antigens in shaping, tuning, and regulating the autopathogenic T cell repertoire. Annu. Rev. Immunol.20, 101–123 (2002). ArticleCASPubMed Google Scholar
Ferber, I.A. et al. Mice with a disrupted IFN-gamma gene are susceptible to the induction of experimental autoimmune encephalomyelitis (EAE). J. Immunol.156, 5–7 (1996). CASPubMed Google Scholar
Wildbaum, G., Youssef, S., Grabie, N. & Karin, N. Neutralizing antibodies to IFN-γ-inducing factor prevent experimental autoimmune encephalomyelitis. J. Immunol.161, 6368–6374 (1998). CASPubMed Google Scholar
Bettelli, E. et al. Loss of T-bet, but not STAT1, prevents the development of experimental autoimmune encephalomyelitis. J. Exp. Med.200, 79–87 (2004). ArticleCASPubMedPubMed Central Google Scholar
Bettelli, E. et al. Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells. Nature441, 235–238 (2006). ArticleCASPubMed Google Scholar
Mangan, P.R. et al. Transforming growth factor-β induces development of the TH17 lineage. Nature441, 231–234 (2006). ArticleCASPubMed Google Scholar
Veldhoen, M., Hocking, R.J., Atkins, C.J., Locksley, R.M. & Stockinger, B. TGFβ in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells. Immunity24, 179–189 (2006). ArticleCASPubMed Google Scholar
Korn, T., Bettelli, E., Oukka, M. & Kuchroo, V.K. IL-17 and Th17 cells. Annu. Rev. Immunol.27, 485–517 (2009). ArticleCASPubMed Google Scholar
Ivanov, I.I. et al. The orphan nuclear receptor RORγt directs the differentiation program of proinflammatory IL-17+ T helper cells. Cell126, 1121–1133 (2006). ArticleCASPubMed Google Scholar
Awasthi, A. et al. Cutting edge: IL-23 receptor gfp reporter mice reveal distinct populations of IL-17-producing cells. J. Immunol.182, 5904–5908 (2009). ArticleCASPubMed Google Scholar
Cua, D.J. et al. Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brain. Nature421, 744–748 (2003). ArticleCASPubMed Google Scholar
McGeachy, M.J. et al. The interleukin 23 receptor is essential for the terminal differentiation of interleukin 17–producing effector T helper cells in vivo. Nat. Immunol.10, 314–324 (2009). ArticleCASPubMedPubMed Central Google Scholar
Duerr, R.H. et al. A genome-wide association study identifies IL23R as an inflammatory bowel disease gene. Science314, 1461–1463 (2006). ArticleCASPubMedPubMed Central Google Scholar
Rahman, P. et al. Association of interleukin-23 receptor variants with ankylosing spondylitis. Arthritis Rheum.58, 1020–1025 (2008). ArticleCASPubMed Google Scholar
McGeachy, M.J. et al. TGF-β and IL-6 drive the production of IL-17 and IL-10 by T cells and restrain TH-17 cell-mediated pathology. Nat. Immunol.8, 1390–1397 (2007). ArticleCASPubMed Google Scholar
Jäger, A., Dardalhon, V., Sobel, R.A., Bettelli, E. & Kuchroo, V.K. Th1, Th17, and Th9 effector cells induce experimental autoimmune encephalomyelitis with different pathological phenotypes. J. Immunol.183, 7169–7177 (2009). ArticlePubMed Google Scholar
Codarri, L. et al. RORγt drives production of the cytokine GM-CSF in helper T cells, which is essential for the effector phase of autoimmune neuroinflammation. Nat. Immunol.12, 560–567 (2011). ArticleCASPubMed Google Scholar
El-Behi, M. et al. The encephalitogenicity of TH17 cells is dependent on IL-1- and IL-23-induced production of the cytokine GM-CSF. Nat. Immunol.12, 568–575 (2011). ArticleCASPubMedPubMed Central Google Scholar
McQualter, J.L. et al. Granulocyte macrophage colony-stimulating factor: a new putative therapeutic target in multiple sclerosis. J. Exp. Med.194, 873–882 (2001). ArticleCASPubMedPubMed Central Google Scholar
Lyons, R.M., Miller, D.A., Graycar, J.L., Moses, H.L. & Derynck, R. Differential binding of transforming growth factor-β1, -β2, and -β3 by fibroblasts and epithelial cells measured by affinity cross-linking of cell surface receptors. Mol. Endocrinol.5, 1887–1896 (1991). ArticleCASPubMed Google Scholar
Graycar, J.L. et al. Human transforming growth factor-β3: recombinant expression, purification, and biological activities in comparison with transforming growth factors-β1 and -β2. Mol. Endocrinol.3, 1977–1986 (1989). ArticleCASPubMed Google Scholar
Veldhoen, M., Hocking, R.J., Flavell, R.A. & Stockinger, B. Signals mediated by transforming growth factor-β initiate autoimmune encephalomyelitis, but chronic inflammation is needed to sustain disease. Nat. Immunol.7, 1151–1156 (2006). ArticleCASPubMed Google Scholar
O'Connor, R.A. et al. Cutting edge: Th1 cells facilitate the entry of Th17 cells to the central nervous system during experimental autoimmune encephalomyelitis. J. Immunol.181, 3750–3754 (2008). CASPubMed Google Scholar
Gocke, A.R. et al. T-bet regulates the fate of Th1 and Th17 lymphocytes in autoimmunity. J. Immunol.178, 1341–1348 (2007). ArticleCASPubMed Google Scholar
Park, I.K., Shultz, L.D., Letterio, J.J. & Gorham, J.D. TGF-β1 inhibits T-bet induction by IFN-γ in murine CD4+ T cells through the protein tyrosine phosphatase Src homology region 2 domain-containing phosphatase-1. J. Immunol.175, 5666–5674 (2005). ArticleCASPubMed Google Scholar
Zhou, L. et al. IL-6 programs TH-17 cell differentiation by promoting sequential engagement of the IL-21 and IL-23 pathways. Nat. Immunol.8, 967–974 (2007). ArticleCASPubMed Google Scholar
Walline, C.C., Kanakasabai, S. & Bright, J.J. IL-7Rα confers susceptibility to experimental autoimmune encephalomyelitis. Genes Immun.12, 1–14 (2011). ArticleCASPubMed Google Scholar
Liu, X. et al. Crucial role of interleukin-7 in T helper type 17 survival and expansion in autoimmune disease. Nat. Med.16, 191–197 (2010). ArticleCASPubMed Google Scholar
Lundmark, F. et al. Variation in interleukin 7 receptor α chain (IL7R) influences risk of multiple sclerosis. Nat. Genet.39, 1108–1113 (2007). ArticleCASPubMed Google Scholar
Gregory, S.G. et al. Interleukin 7 receptor α chain (IL7R) shows allelic and functional association with multiple sclerosis. Nat. Genet.39, 1083–1091 (2007). ArticleCASPubMed Google Scholar
Veldhoen, M. et al. The aryl hydrocarbon receptor links TH17-cell-mediated autoimmunity to environmental toxins. Nature453, 106–109 (2008). ArticleCASPubMed Google Scholar
Quintana, F.J. et al. Control of Treg and TH17 cell differentiation by the aryl hydrocarbon receptor. Nature453, 65–71 (2008). ArticleCASPubMed Google Scholar
Bauquet, A.T. et al. The costimulatory molecule ICOS regulates the expression of c-Maf and IL-21 in the development of follicular T helper cells and TH-17 cells. Nat. Immunol.10, 167–175 (2008). ArticlePubMedPubMed Central Google Scholar
Apetoh, L. et al. The aryl hydrocarbon receptor interacts with c-Maf to promote the differentiation of type 1 regulatory T cells induced by IL-27. Nat. Immunol.11, 854–861 (2010). ArticleCASPubMedPubMed Central Google Scholar
Zielinski, C.E. et al. Pathogen-induced human TH17 cells produce IFN-γ or IL-10 and are regulated by IL-1β. Nature484, 514–518 (2012). ArticleCASPubMed Google Scholar
Awasthi, A. et al. A dominant function for interleukin 27 in generating interleukin 10-producing anti-inflammatory T cells. Nat. Immunol.8, 1380–1389 (2007). ArticleCASPubMed Google Scholar
Irizarry, R.A. et al. Exploration, normalization, and summaries of high density oligonucleotide array probe level data. Biostatistics4, 249–264 (2003). ArticlePubMed Google Scholar
Johnson, W.E., Li, C. & Rabinovic, A. Adjusting batch effects in microarray expression data using empirical Bayes methods. Biostatistics8, 118–127 (2007). ArticlePubMed Google Scholar