IL-6-deficient mice are resistant to the induction of experimental autoimmune encephalomyelitis provoked by myelin oligodendrocyte glycoprotein

作者：Yusuke Okuda · 发表于：International Immunology · 年份：1998 · DOI：10.1093/intimm/10.5.703 · 被引用次数：230 · 研究领域：Cytokine Signaling Pathways and Interactions、Multiple Sclerosis Research Studies、Systemic Lupus Erythematosus Research

The role of IL-6 in experimental autoimmune encephalomyelitis (EAE) provoked by myelin oligodendrocyte glycoprotein (MOG) was investigated using IL-6-deficient mice. We show here that IL-6-deficient mice were resistant to the MOG-induced EAE as compared to wild-type mice (one out of 18 versus 17 out of 20). The delayed-type hypersensitivity response, lymphocyte proliferation response and antibody reactivity to MOG in IL-6-deficient mice were significantly lower than those in wild-type mice. Furthermore, the histological examination revealed that no infiltration of inflammatory cells was observed in the central nervous system of IL-6-deficient mice. These results indicate that IL-6 may play a crucial role in the induction phase of EAE. Given the potential relevance of this animal model for multiple sclerosis (MS), it is possible that anti-IL-6 therapy may be useful in the prevention of relapses of MS.