Anti-IL-17A blocking antibody reduces cyclosporin A-induced relapse in experimental autoimmune encephalomyelitis mice |
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Authors: | Kodai Saitoh Shigeyuki Kon Takuya Nakatsuru Kyosuke Inui Takeru Ihara Naoki Matsumoto Yuichi Kitai Ryuta Muromoto Tadashi Matsuda |
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Affiliation: | 1. Department of Immunology, Faculty of Pharmaceutical Sciences, Hokkaido University, Kita-15, Nishi-7, Kita-ku, Sapporo 060-0815, Japan;2. Department of Molecular Immunology, Faculty of Pharmaceutical Sciences, Fukuyama University, Fukuyama 729-0292, Japan |
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Abstract: | Cyclosporin A (CsA) is effective at reducing pathogenic immune responses, but upon withdrawal of CsA the immune response often “rebounds” resulting in a relapse or exacerbation of disease. The mechanisms, cells and cytokines involved in the relapse or exacerbation after CsA withdrawal are unknown. We hypothesized that CsA withdrawal induces IL-17 production that could be responsible for relapse, and examined the effect of anti-IL-17A antibody on relapse induced after CsA withdrawal in mouse experimental autoimmune encephalomyelitis (EAE). CsA treatment markedly decreased the EAE disease score during the first episode, but augmented disease severity after CsA withdrawal, compared to untreated mice. After discontinuation of CsA the production of IL-17A was increased and the severity of relapse in EAE was reduced by treatment with anti-IL-17A antibody. These results suggest that the resumption of T cell immune responses after CsA withdrawal leads to a burst of IL-17A production that is at least partially responsible for relapse in EAE mice. |
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Keywords: | IL-17A Experimental autoimmune encephalomyelitis (EAE) Relapse Cyclosporin A (CsA) |
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