| First Author | Zhou X | Year | 2011 |
| Journal | PLoS One | Volume | 6 |
| Issue | 8 | Pages | e23629 |
| PubMed ID | 21897850 | Mgi Jnum | J:176143 |
| Mgi Id | MGI:5288545 | Doi | 10.1371/journal.pone.0023629 |
| Citation | Zhou X, et al. (2011) BAFF Promotes Th17 Cells and Aggravates Experimental Autoimmune Encephalomyelitis. PLoS One 6(8):e23629 |
| abstractText | BACKGROUND: BAFF, in addition to promoting B cell survival and differentiation, may affect T cells. The objective of this study was to determine the effect of BAFF on Th17 cell generation and its ramifications for the Th17 cell-driven disease, EAE. METHODOLOGY/PRINCIPAL FINDINGS: Th17 cells were increased in BAFF-Tg B6 (B6.BTg) mice and decreased in B6.Baff(-/-) mice. Th17 cells in B6.Baff(-/-) mice bearing a BAFF Tg (B6.Baff(-/-).BTg mice) were identical to those in B6.BTg mice, indicating that membrane BAFF is dispensable for Th17 cell generation as long as soluble BAFF is plentiful. In T + non-T cell criss-cross co-cultures, Th17 cell generation was greatest in cultures containing B6.BTg T cells and lowest in cultures containing B6.Baff(-/-) T cells, regardless of the source of non-T cells. In cultures containing only T cells, Th17 cell generation followed an identical pattern. CD4(+) cell expression of CD126 (IL-6R alpha chain) was increased in B6.BTg mice and decreased in B6.Baff(-/-) mice, and activation of STAT3 following stimulation with IL-6 + TGF-beta was also greatest in B6.BTg cells and lowest in B6.Baff(-/-) cells. EAE was clinically and pathologically most severe in B6.BTg mice and least severe in B6.Baff(-/-) mice and correlated with MOG(35-55) peptide-induced Th17 cell responses. CONCLUSIONS/SIGNIFICANCE: Collectively, these findings document a contribution of BAFF to pathogenic Th17 cell responses and suggest that BAFF antagonism may be efficacious in Th17 cell-driven diseases. |
