Journal
SCIENTIFIC REPORTS
Volume 6, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/srep34594
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Funding
- Swiss National Science Foundation [PP00P3_152928, 310030_153164]
- Klaus-Tschira Foundation
- Helmut Horten Foundation
- Gebert-Ruf Foundation
- Swiss MS Society
- National Multiple Sclerosis Society (NMSS) [PP 1660]
- DFG [WE 3547/4-1]
- ProFutura Programm of the Universitatsmedizin Gottingen
- National Health and Medical Research Council of Australia [APP1053621]
- Department of Industry, Commonwealth of Australia [AISRF06680]
- Swiss MS Society (SMSS)
- European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) Foundation
- SMSS
- Swiss National Science Foundation (SNF) [310030_153164, PP00P3_152928] Funding Source: Swiss National Science Foundation (SNF)
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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)-beta 1 expression in regulatory B cell functions, this mechanism has not yet been tested in autoimmune neuroinflammation. Transgenic mice deficient for TGF-beta 1 expression in B cells (B-TGF-beta 1(-/-)) were tested in EAE induced by recombinant mouse myelin oligodendrocyte glycoprotein (rmMOG). In this model, B-TGF-beta 1(-/-) mice showed an earlier onset of neurologic impairment compared to their littermate controls. Exacerbated EAE susceptibility in B-TGF-beta 1(-/-) mice was associated with augmented CNS T helper (Th) 1/17 responses. Moreover, selective B cell TGF-beta 1-deficiency increased the frequencies and activation of myeloid dendritic cells, potent professional antigen-presenting cells (APCs), suggesting that B cell-derived TGF-beta 1 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-beta 1, findings that may be relevant to B cell-targeted therapies.
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