Dong, C. TH17 cells in development: an updated view of their molecular identity and genetic programming. Nat. Rev. Immunol.8, 337–348 (2008). ArticleCASPubMed Google Scholar
Weaver, C.T., Hatton, R.D., Mangan, P.R. & Harrington, L.E. IL-17 family cytokines and the expanding diversity of effector T cell lineages. Annu. Rev. Immunol.25, 821–852 (2007). ArticleCASPubMed Google Scholar
Steinman, L. A brief history of TH17, the first major revision in the TH1/TH2 hypothesis of T cell-mediated tissue damage. Nat. Med.13, 139–145 (2007). 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
Komiyama, Y. et al. IL-17 plays an important role in the development of experimental autoimmune encephalomyelitis. J. Immunol.177, 566–573 (2006). ArticleCASPubMed Google Scholar
Hofstetter, H.H. et al. Therapeutic efficacy of IL-17 neutralization in murine experimental autoimmune encephalomyelitis. Cell. Immunol.237, 123–130 (2005). ArticleCASPubMed Google Scholar
Langrish, C.L. et al. IL-23 drives a pathogenic T cell population that induces autoimmune inflammation. J. Exp. Med.201, 233–240 (2005). ArticleCASPubMedPubMed Central Google Scholar
Tzartos, J.S. et al. Interleukin-17 production in central nervous system-infiltrating T cells and glial cells is associated with active disease in multiple sclerosis. Am. J. Pathol.172, 146–155 (2008). ArticleCASPubMedPubMed Central 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
Luger, D. et al. Either a Th17 or a Th1 effector response can drive autoimmunity: conditions of disease induction affect dominant effector category. J. Exp. Med.205, 799–810 (2008). ArticleCASPubMedPubMed Central Google Scholar
Kroenke, M.A., Carlson, T.J., Andjelkovic, A.V. & Segal, B.M. IL-12- and IL-23-modulated T cells induce distinct types of EAE based on histology, CNS chemokine profile, and response to cytokine inhibition. J. Exp. Med.205, 1535–1541 (2008). ArticleCASPubMedPubMed Central Google Scholar
Stromnes, I.M., Cerretti, L.M., Liggitt, D., Harris, R.A. & Goverman, J.M. Differential regulation of central nervous system autoimmunity by TH1 and TH17 cells. Nat. Med.14, 337–342 (2008). ArticleCASPubMedPubMed Central Google Scholar
Lees, J.R., Golumbek, P.T., Sim, J., Dorsey, D. & Russell, J.H. Regional CNS responses to IFN-γ determine lesion localization patterns during EAE pathogenesis. J. Exp. Med.205, 2633–2642 (2008). ArticleCASPubMedPubMed Central Google Scholar
Engelhardt, B. & Ransohoff, R.M. The ins and outs of T-lymphocyte trafficking to the CNS: anatomical sites and molecular mechanisms. Trends Immunol.26, 485–495 (2005). ArticleCASPubMed Google Scholar
Yednock, T.A. et al. Prevention of experimental autoimmune encephalomyelitis by antibodies against α4β1 integrin. Nature356, 63–66 (1992). ArticleCASPubMed Google Scholar
Engelhardt, B., Vestweber, D., Hallmann, R. & Schulz, M. E- and P-selectin are not involved in the recruitment of inflammatory cells across the blood-brain barrier in experimental autoimmune encephalomyelitis. Blood90, 4459–4472 (1997). CASPubMed Google Scholar
Carrithers, M.D., Visintin, I., Kang, S.J. & Janeway, C.A. Jr. Differential adhesion molecule requirements for immune surveillance and inflammatory recruitment. Brain123, 1092–1101 (2000). ArticlePubMed Google Scholar
Piccio, L. et al. Molecular mechanisms involved in lymphocyte recruitment in inflamed brain microvessels: critical roles for P-selectin glycoprotein ligand-1 and heterotrimeric Gi-linked receptors. J. Immunol.168, 1940–1949 (2002). ArticleCASPubMed Google Scholar
Vajkoczy, P., Laschinger, M. & Engelhardt, B. α4-integrin-VCAM-1 binding mediates G protein-independent capture of encephalitogenic T cell blasts to CNS white matter microvessels. J. Clin. Invest.108, 557–565 (2001). ArticleCASPubMedPubMed Central Google Scholar
Engelhardt, B., Wolburg-Buchholz, K. & Wolburg, H. Involvement of the choroid plexus in central nervous system inflammation. Microsc. Res. Tech.52, 112–129 (2001). ArticleCASPubMed Google Scholar
Ransohoff, R.M., Kivisakk, P. & Kidd, G. Three or more routes for leukocyte migration into the central nervous system. Nat. Rev. Immunol.3, 569–581 (2003). ArticleCASPubMed Google Scholar
Giunti, D. et al. Phenotypic and functional analysis of T cells homing into the CSF of subjects with inflammatory diseases of the CNS. J. Leukoc. Biol.73, 584–590 (2003). ArticleCASPubMed Google Scholar
Steffen, B.J., Breier, G., Butcher, E.C., Schulz, M. & Engelhardt, B. ICAM-1, VCAM-1, and MAdCAM-1 are expressed on choroid plexus epithelium but not endothelium and mediate binding of lymphocytes in vitro. Am. J. Pathol.148, 1819–1838 (1996). CASPubMedPubMed Central Google Scholar
Pedemonte, E. et al. Mechanisms of the adaptive immune response inside the central nervous system during inflammatory and autoimmune diseases. Pharmacol. Ther.111, 555–566 (2006). ArticleCASPubMed Google Scholar
Bromley, S.K., Mempel, T.R. & Luster, A.D. Orchestrating the orchestrators: chemokines in control of T cell traffic. Nat. Immunol.9, 970–980 (2008). ArticleCASPubMed Google Scholar
Rossi, D.L., Vicari, A.P., Franz-Bacon, K., McClanahan, T.K. & Zlotnik, A. Identification through bioinformatics of two new macrophage proinflammatory human chemokines: MIP-3α and MIP-3β. J. Immunol.158, 1033–1036 (1997). CASPubMed Google Scholar
Acosta-Rodriguez, E.V. et al. Surface phenotype and antigenic specificity of human interleukin 17–producing T helper memory cells. Nat. Immunol.8, 639–646 (2007). ArticleCASPubMed Google Scholar
Cook, D.N. et al. CCR6 mediates dendritic cell localization, lymphocyte homeostasis, and immune responses in mucosal tissue. Immunity12, 495–503 (2000). ArticleCASPubMed Google Scholar
Greaves, D.R. et al. CCR6, a CC chemokine receptor that interacts with macrophage inflammatory protein 3α and is highly expressed in human dendritic cells. J. Exp. Med.186, 837–844 (1997). ArticleCASPubMedPubMed Central Google Scholar
Brown, D.A. & Sawchenko, P.E. Time course and distribution of inflammatory and neurodegenerative events suggest structural bases for the pathogenesis of experimental autoimmune encephalomyelitis. J. Comp. Neurol.502, 236–260 (2007). ArticlePubMed Google Scholar
Kivisakk, P. et al. Localizing central nervous system immune surveillance: Meningeal antigen-presenting cells activate T cells during experimental autoimmune encephalomyelitis. Ann. Neurol. published online, doi:10.1002/ana.21379 (21 May 2008).
Hickey, W.F., Hsu, B.L. & Kimura, H. T-lymphocyte entry into the central nervous system. J. Neurosci. Res.28, 254–260 (1991). ArticleCASPubMed Google Scholar
Flugel, A. et al. Migratory activity and functional changes of green fluorescent effector cells before and during experimental autoimmune encephalomyelitis. Immunity14, 547–560 (2001). ArticleCASPubMed Google Scholar
Hirota, K. et al. Preferential recruitment of CCR6-expressing Th17 cells to inflamed joints via CCL20 in rheumatoid arthritis and its animal model. J. Exp. Med.204, 2803–2812 (2007). ArticleCASPubMedPubMed Central Google Scholar
Khader, S.A. et al. IL-23 and IL-17 in the establishment of protective pulmonary CD4+ T cell responses after vaccination and during Mycobacterium tuberculosis challenge. Nat. Immunol.8, 369–377 (2007). ArticleCASPubMed Google Scholar
Steinman, L. A few autoreactive cells in an autoimmune infiltrate control a vast population of nonspecific cells: a tale of smart bombs and the infantry. Proc. Natl. Acad. Sci. USA93, 2253–2256 (1996). ArticleCASPubMedPubMed Central 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). ArticleCASPubMed Google Scholar
Kebir, H. et al. Human TH17 lymphocytes promote blood-brain barrier disruption and central nervous system inflammation. Nat. Med.13, 1173–1175 (2007). ArticleCASPubMedPubMed Central Google Scholar
Kreymborg, K. et al. IL-22 is expressed by Th17 cells in an IL-23-dependent fashion, but not required for the development of autoimmune encephalomyelitis. J. Immunol.179, 8098–8104 (2007). ArticleCASPubMed Google Scholar
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). CASPubMed Google Scholar
Charo, I.F. & Ransohoff, R.M. The many roles of chemokines and chemokine receptors in inflammation. N. Engl. J. Med.354, 610–621 (2006). ArticleCASPubMed Google Scholar
Balashov, K.E., Rottman, J.B., Weiner, H.L. & Hancock, W.W. CCR5+ and CXCR3+ T cells are increased in multiple sclerosis and their ligands MIP-1α and IP-10 are expressed in demyelinating brain lesions. Proc. Natl. Acad. Sci. USA96, 6873–6878 (1999). ArticleCASPubMedPubMed Central Google Scholar
Ambrosini, E., Columba-Cabezas, S., Serafini, B., Muscella, A. & Aloisi, F. Astrocytes are the major intracerebral source of macrophage inflammatory protein-3α/CCL20 in relapsing experimental autoimmune encephalomyelitis and in vitro. Glia41, 290–300 (2003). ArticlePubMed Google Scholar
Columba-Cabezas, S., Serafini, B., Ambrosini, E. & Aloisi, F. Lymphoid chemokines CCL19 and CCL21 are expressed in the central nervous system during experimental autoimmune encephalomyelitis: implications for the maintenance of chronic neuroinflammation. Brain Pathol.13, 38–51 (2003). ArticlePubMed Google Scholar
Rottman, J.B. et al. Leukocyte recruitment during onset of experimental allergic encephalomyelitis is CCR1 dependent. Eur. J. Immunol.30, 2372–2377 (2000). ArticleCASPubMed Google Scholar
Muller, M. et al. CXCR3 signaling reduces the severity of experimental autoimmune encephalomyelitis by controlling the parenchymal distribution of effector and regulatory T cells in the central nervous system. J. Immunol.179, 2774–2786 (2007). ArticlePubMed Google Scholar
Liu, L. et al. Severe disease, unaltered leukocyte migration, and reduced IFN-γ production in CXCR3−/− mice with experimental autoimmune encephalomyelitis. J. Immunol.176, 4399–4409 (2006). ArticleCASPubMed Google Scholar
Gaupp, S., Pitt, D., Kuziel, W.A., Cannella, B. & Raine, C.S. Experimental autoimmune encephalomyelitis (EAE) in CCR2−/− mice: susceptibility in multiple strains. Am. J. Pathol.162, 139–150 (2003). ArticlePubMedPubMed Central Google Scholar
Eltayeb, S. et al. Temporal expression and cellular origin of CC chemokine receptors CCR1, CCR2 and CCR5 in the central nervous system: insight into mechanisms of MOG-induced EAE. J. Neuroinflammation4, 14 (2007). ArticlePubMedPubMed Central Google Scholar
Matsui, M. et al. Treatment of experimental autoimmune encephalomyelitis with the chemokine receptor antagonist Met-RANTES. J. Neuroimmunol.128, 16–22 (2002). ArticleCASPubMed Google Scholar
Kohler, R.E., Caon, A.C., Willenborg, D.O., Clark-Lewis, I. & McColl, S.R. A role for macrophage inflammatory protein-3α/CC chemokine ligand 20 in immune priming during T cell-mediated inflammation of the central nervous system. J. Immunol.170, 6298–6306 (2003). ArticleCASPubMed Google Scholar
Franciotta, D., Salvetti, M., Lolli, F., Serafini, B. & Aloisi, F. B cells and multiple sclerosis. Lancet Neurol.7, 852–858 (2008). ArticleCASPubMed Google Scholar
Kleinewietfeld, M. et al. CCR6 expression defines regulatory effector/memory-like cells within the CD25+CD4+ T-cell subset. Blood105, 2877–2886 (2005). ArticleCASPubMed Google Scholar
Yamazaki, T. et al. CCR6 regulates the migration of inflammatory and regulatory T cells. J. Immunol.181, 8391–8401 (2008). ArticleCASPubMed Google Scholar
Sigmundsdottir, H. & Butcher, E.C. Environmental cues, dendritic cells and the programming of tissue-selective lymphocyte trafficking. Nat. Immunol.9, 981–987 (2008). ArticleCASPubMedPubMed Central Google Scholar
Hickey, W.F. Basic principles of immunological surveillance of the normal central nervous system. Glia36, 118–124 (2001). ArticleCASPubMed Google Scholar