Abstract
Dectin-1, the receptor for beta-glucans, protects host from fungal infection. However, the role of Dectin-1 in intestinal immunity has not been elucidated completely. We found that Dectin-1-deficient (Clec7a−/−) mice were refractory to both dextran sodium sulfate (DSS)- and CD45RBhiCD4+ T cell-induced colitis associated with an increase of regulatory T (Treg) cells. The proportion of lactobacilli, especially Lactobacillus murinus (L. murinus), in commensal microflora was increased in Clec7a−/− mouse colon due to accompanied by a decrease of a group of antimicrobial peptides induced by Dectin-1 signaling. L. murinus colonization increased Treg cells in the colon. Oral administration of laminarin, a Dectin-1 antagonist, suppressed the development of DSS-colitis, associated with the increase of L. murinus and Treg cells. The proportion of closely related Lactobacillus species was decreased in inflammatory bowel disease patients. These observations suggest that Dectin-1 regulates the homeostasis of intestinal immunity by controlling Treg cell differentiation through modification of microbiota.
Published Version
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