BAFF promotes Th17 cells and aggravates experimental autoimmune encephalomyelitis.

<h4>Background</h4>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.<h4>Methodology/principal f...

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Main Authors: Xiaohui Zhou, Zanxian Xia, Qin Lan, Julie Wang, Wenru Su, Yuan-Ping Han, Huimin Fan, Zhongmin Liu, William Stohl, Song Guo Zheng
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2011-01-01
Series:PLoS ONE
Online Access:https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0023629&type=printable
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author Xiaohui Zhou
Zanxian Xia
Qin Lan
Julie Wang
Wenru Su
Yuan-Ping Han
Huimin Fan
Zhongmin Liu
William Stohl
Song Guo Zheng
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
collection DOAJ
description <h4>Background</h4>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.<h4>Methodology/principal findings</h4>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.<h4>Conclusions/significance</h4>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.
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publisher Public Library of Science (PLoS)
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spelling doaj-art-1c14bde876fc49a98ed86a1e6302ecd02025-08-20T03:09:48ZengPublic 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 Zheng<h4>Background</h4>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.<h4>Methodology/principal findings</h4>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.<h4>Conclusions/significance</h4>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.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0023629&type=printable
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
title 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_short BAFF promotes Th17 cells and aggravates experimental autoimmune encephalomyelitis.
title_sort baff promotes th17 cells and aggravates experimental autoimmune encephalomyelitis
url https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0023629&type=printable
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