Abstract
Abstract Dectin-1 (encoded by Clec7a) is a mainly myeloid cell-expressed natural killer (NK)-cell-receptor-like C-type lectin that functions as a fungal recognition receptor by binding to b-glucan carbohydrates. However, the role of Dectin-1 in adaptive immunity is not fully understood. In this study, we surprisingly found that mice deficient for Dectin-1 develop severe experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS). The heightened EAE severity observed in Clec7a−/− mice correlates with increased Th17 response in the draining lymph nodes. Further analysis showed that Clec7a−/− mice have a reduced regulatory CD8+ T cells, a newly discovered CD8+ T cell subset defined as the surface expression of CD8, CD44, CD122, and Ly49+, which have been shown to suppress EAE development. In support of a critical role of Dectin-1 in non-CD4+ T cells in the development of EAE, Tcrb−/− mice receiving wild-type and Clec7a−/− CD4+ T cells develop a comparable degree of EAE. Therefore, our data suggest that Dectin-1 regulates EAE development possibly via controlling regulatory CD8+ T cell development.
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