BAFF promotes Th17 cells and aggravates experimental autoimmune encephalomyelitis.
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.Th17 cells were increased in BAFF-Tg B6 (B6.BTg) mice and decrea...
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doaj-1c14bde876fc49a98ed86a1e6302ecd02020-11-24T21:34:05ZengPublic Library of Science (PLoS)PLoS ONE1932-62032011-01-0168e2362910.1371/journal.pone.0023629BAFF promotes Th17 cells and aggravates experimental autoimmune encephalomyelitis.Xiaohui ZhouZanxian XiaQin LanJulie WangWenru SuYuan-Ping HanHuimin FanZhongmin LiuWilliam StohlSong Guo ZhengBAFF, 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.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 α chain) was increased in B6.BTg mice and decreased in B6.Baff(-/-) mice, and activation of STAT3 following stimulation with IL-6 + TGF-β 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.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.http://europepmc.org/articles/PMC3163640?pdf=render |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Xiaohui Zhou Zanxian Xia Qin Lan Julie Wang Wenru Su Yuan-Ping Han Huimin Fan Zhongmin Liu William Stohl Song Guo Zheng |
spellingShingle |
Xiaohui Zhou Zanxian Xia Qin Lan Julie Wang Wenru Su Yuan-Ping Han Huimin Fan Zhongmin Liu William Stohl Song Guo Zheng BAFF promotes Th17 cells and aggravates experimental autoimmune encephalomyelitis. PLoS ONE |
author_facet |
Xiaohui Zhou Zanxian Xia Qin Lan Julie Wang Wenru Su Yuan-Ping Han Huimin Fan Zhongmin Liu William Stohl Song Guo Zheng |
author_sort |
Xiaohui Zhou |
title |
BAFF promotes Th17 cells and aggravates experimental autoimmune encephalomyelitis. |
title_short |
BAFF promotes Th17 cells and aggravates experimental autoimmune encephalomyelitis. |
title_full |
BAFF promotes Th17 cells and aggravates experimental autoimmune encephalomyelitis. |
title_fullStr |
BAFF promotes Th17 cells and aggravates experimental autoimmune encephalomyelitis. |
title_full_unstemmed |
BAFF promotes Th17 cells and aggravates experimental autoimmune encephalomyelitis. |
title_sort |
baff promotes th17 cells and aggravates experimental autoimmune encephalomyelitis. |
publisher |
Public Library of Science (PLoS) |
series |
PLoS ONE |
issn |
1932-6203 |
publishDate |
2011-01-01 |
description |
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.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 α chain) was increased in B6.BTg mice and decreased in B6.Baff(-/-) mice, and activation of STAT3 following stimulation with IL-6 + TGF-β 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.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. |
url |
http://europepmc.org/articles/PMC3163640?pdf=render |
work_keys_str_mv |
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