Arnason, B.G. Immunologic therapy of multiple sclerosis. Annu. Rev. Med. 50, 291–302 (1999).
Wang, A.G., Lin, Y.C., Wang, S.J., Tsai, C.P. & Yen, M.Y. Early relapse in multiple sclerosis–associated optic neuritis following the use of interferon β-1a in Chinese patients. Jpn. J. Ophthalmol. 50, 537–542 (2006).
Benveniste, E.N. & Qin, H. Type I interferons as anti-inflammatory mediators. Sci. STKE 2007, pe70 (2007).
Prinz, M. et al. Distinct and nonredundant in vivo functions of IFNAR on myeloid cells limit autoimmunity in the central nervous system. Immunity 28, 675–686 (2008).
Guo, B., Chang, E.Y. & Cheng, G. The type I IFN induction pathway constrains TH17-mediated autoimmune inflammation in mice. J. Clin. Invest. 118, 1680–1690 (2008).
Nagai, T., Devergne, O., van Seventer, G.A. & van Seventer, J.M. Interferon-β mediates opposing effects on interferon-γ–dependent interleukin-12 p70 secretion by human monocyte-derived dendritic cells. Scand. J. Immunol. 65, 107–117 (2007).
McRae, B.L., Semnani, R.T., Hayes, M.P., van Seventer, G.A. & Type, I. IFNs inhibit human dendritic cell IL-12 production and TH1 cell development. J. Immunol. 160, 4298–4304 (1998).
Martín-Saavedra, F.M., Gonzalez-Garcia, C., Bravo, B. & Ballester, S. β interferon restricts the inflammatory potential of CD4+ cells through the boost of the TH2 phenotype, the inhibition of TH17 response and the prevalence of naturally occurring T regulatory cells. Mol. Immunol. 45, 4008–4019 (2008).
Langrish, C.L. et al. IL-23 drives a pathogenic T cell population that induces autoimmune inflammation. J. Exp. Med. 201, 233–240 (2005).
Fitzgerald, D.C. et al. Suppression of autoimmune inflammation of the central nervous system by interleukin 10 secreted by interleukin 27–stimulated T cells. Nat. Immunol. 8, 1372–1379 (2007).
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. Immunity 24, 179–189 (2006).
Mangan, P.R. et al. Transforming growth factor-β induces development of the TH17 lineage. Nature 441, 231–234 (2006).
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).
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).
Platanias, L.C. Mechanisms of type-I- and type-II-interferon–mediated signalling. Nat. Rev. Immunol. 5, 375–386 (2005).
Nguyen, K.B. et al. Interferon α/β–mediated inhibition and promotion of interferon γ: STAT1 resolves a paradox. Nat. Immunol. 1, 70–76 (2000).
Tanabe, Y. et al. Cutting edge: role of STAT1, STAT3, and STAT5 in IFN-α β responses in T lymphocytes. J. Immunol. 174, 609–613 (2005).
Wong, L.H., Hatzinisiriou, I., Devenish, R.J. & Ralph, S.J. IFN-γ priming up-regulates IFN-stimulated gene factor 3 (ISGF3) components, augmenting responsiveness of IFN-resistant melanoma cells to type I IFNs. J. Immunol. 160, 5475–5484 (1998).
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).
Berenson, L.S., Gavrieli, M., Farrar, J.D., Murphy, T.L. & Murphy, K.M. Distinct characteristics of murine STAT4 activation in response to IL-12 and IFN-α. J. Immunol. 177, 5195–5203 (2006).
Parronchi, P. et al. IL-4 and IFN (α and γ) exert opposite regulatory effects on the development of cytolytic potential by TH1 or TH2 human T cell clones. J. Immunol. 149, 2977–2983 (1992).
Bettelli, E. et al. Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells. Nature 441, 235–238 (2006).
Graber, J.J. et al. Cytokine changes during interferon-β therapy in multiple sclerosis: correlations with interferon dose and MRI response. J. Neuroimmunol. 185, 168–174 (2007).
Bartosik-Psujek, H. & Stelmasiak, Z. The interleukin-10 levels as a potential indicator of positive response to interferon β treatment of multiple sclerosis patients. Clin. Neurol. Neurosurg. 108, 644–647 (2006).
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).
Harrington, L.E. et al. Interleukin 17–producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages. Nat. Immunol. 6, 1123–1132 (2005).
Haak, S. et al. IL-17A and IL-17F do not contribute vitally to autoimmune neuro-inflammation in mice. J. Clin. Invest. 119, 61–69 (2009).
Lucchinetti, C.F. et al. A role for humoral mechanisms in the pathogenesis of Devic's neuromyelitis optica. Brain 125, 1450–1461 (2002).
Hengstman, G.J., Wesseling, P., Frenken, C.W. & Jongen, P.J. Neuromyelitis optica with clinical and histopathological involvement of the brain. Mult. Scler. 13, 679–682 (2007).
Zhang, Z. et al. Interleukin-17 causes neutrophil mediated inflammation in ovalbumin-induced uveitis in DO11.10 mice. Cytokine 46, 79–91 (2009).
Liang, S.C. et al. An IL-17F/A heterodimer protein is produced by mouse TH17 cells and induces airway neutrophil recruitment. J. Immunol. 179, 7791–7799 (2007).
Smith, E. et al. IL-23 is required for neutrophil homeostasis in normal and neutrophilic mice. J. Immunol. 179, 8274–8279 (2007).
Ishizu, T. et al. Intrathecal activation of the IL-17/IL-8 axis in opticospinal multiple sclerosis. Brain 128, 988–1002 (2005).
Warabi, Y., Matsumoto, Y. & Hayashi, H. Interferon β-1b exacerbates multiple sclerosis with severe optic nerve and spinal cord demyelination. J. Neurol. Sci. 252, 57–61 (2007).
Shimizu, Y. et al. Development of extensive brain lesions following interferon β therapy in relapsing neuromyelitis optica and longitudinally extensive myelitis. J. Neurol. 255, 305–307 (2008).
Eisen, M.B., Spellman, P.T., Brown, P.O. & Botstein, D. Cluster analysis and display of genome-wide expression patterns. Proc. Natl. Acad. Sci. USA 95, 14863–14868 (1998).