Scientific article
Open access

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

Published inScientific reports, vol. 6, 34594
Publication date2016

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 CNS T helper (Th)1/17 responses. Moreover, selective B cell TGF-β1-deficiency increased the frequencies and activation of myeloid dendritic cells, potent professional antigen-presenting cells (APCs), suggesting that B cell-derived TGF-β1 can constrain Th1/17 responses through inhibition of APC activity. Collectively our data suggest that B cells can down-regulate the function of APCs, and in turn encephalitogenic Th1/17 responses, via TGF-β1, findings that may be relevant to B cell-targeted therapies.

Citation (ISO format)
BJARNADOTTIR, Kristbjorg et al. B cell-derived transforming growth factor-β1 expression limits the induction phase of autoimmune neuroinflammation. In: Scientific reports, 2016, vol. 6, p. 34594. doi: 10.1038/srep34594
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Article (Published version)
ISSN of the journal2045-2322

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