B cell-derived transforming growth factor-β1 expression limits the induction phase of autoimmune neuroinflammation.

ABSTRACT: Studies in experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis (MS), have shown that regulatory B cells modulate the course of the disease via the production of suppressive cytokines. While data indicate a role for transforming growth factor (TGF)-β1 expression in regulatory B cell functions, this mechanism has not yet been tested in autoimmune neuroinflammation. Transgenic mice deficient for TGF-β1 expression in B cells (B-TGF-β1^-/-) were tested in EAE induced by recombinant mouse myelin oligodendrocyte glycoprotein (rmMOG). In this model, B-TGF-β1^-/- mice showed an earlier onset of neurologic impairment compared to their littermate controls. Exacerbated EAE susceptibility in B-TGF-β1^-/- mice was associated with augmented

SUBMITTER: Bjarnadottir K 

PROVIDER: S-EPMC5052622 | biostudies-literature | 2016 Oct

REPOSITORIES: biostudies-literature