| First Author | Bjarnadóttir K | Year | 2016 |
| Journal | Sci Rep | Volume | 6 |
| Pages | 34594 | PubMed ID | 27708418 |
| Mgi Jnum | J:254359 | Mgi Id | MGI:6101540 |
| Doi | 10.1038/srep34594 | Citation | Bjarnadottir K, et al. (2016) B cell-derived transforming growth factor-beta1 expression limits the induction phase of autoimmune neuroinflammation. Sci Rep 6:34594 |
| abstractText | 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)-beta1 expression in regulatory B cell functions, this mechanism has not yet been tested in autoimmune neuroinflammation. Transgenic mice deficient for TGF-beta1 expression in B cells (B-TGF-beta1(-/-)) were tested in EAE induced by recombinant mouse myelin oligodendrocyte glycoprotein (rmMOG). In this model, B-TGF-beta1(-/-) mice showed an earlier onset of neurologic impairment compared to their littermate controls. Exacerbated EAE susceptibility in B-TGF-beta1(-/-) mice was associated with augmented CNS T helper (Th)1/17 responses. Moreover, selective B cell TGF-beta1-deficiency increased the frequencies and activation of myeloid dendritic cells, potent professional antigen-presenting cells (APCs), suggesting that B cell-derived TGF-beta1 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-beta1, findings that may be relevant to B cell-targeted therapies. |
