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Bach2 overexpression represses Th9 cell differentiation by suppressing IRF4 expression in systemic lupus erythematosus
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by abnormal activation of T cells and caused by an imbalance in the production and clearance of apoptotic cells. We previously showed that the transcription regulator Bach2 regulated abnormal B‐cell activation in SLE. H...
Autores principales: | , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7876501/ https://www.ncbi.nlm.nih.gov/pubmed/33249782 http://dx.doi.org/10.1002/2211-5463.13050 |
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author | Sheng, Yujun Zhang, Jiali Li, Keke Wang, Hongyan Wang, Wenjun Wen, Leilei Gao, Jinping Tang, Xianfa Tang, Huayang Huang, He Cai, Minglong Yuan, Tao Liu, Lu Zheng, Xiaodong Zhu, Zhengwei Cui, Yong |
author_facet | Sheng, Yujun Zhang, Jiali Li, Keke Wang, Hongyan Wang, Wenjun Wen, Leilei Gao, Jinping Tang, Xianfa Tang, Huayang Huang, He Cai, Minglong Yuan, Tao Liu, Lu Zheng, Xiaodong Zhu, Zhengwei Cui, Yong |
author_sort | Sheng, Yujun |
collection | PubMed |
description | Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by abnormal activation of T cells and caused by an imbalance in the production and clearance of apoptotic cells. We previously showed that the transcription regulator Bach2 regulated abnormal B‐cell activation in SLE. Here, we investigated whether Bach2 was also involved in Th9 cell differentiation in SLE. We found that the proportion of Th9 cells was enhanced in the peripheral blood mononuclear cells (PBMC) of SLE patients. The PBMC and CD4(+) T cells of SLE patients exhibited a decrease of Bach2 expression and an increase of IL‐9 expression. Furthermore, Bach2 overexpression significantly repressed the levels of PU.1, IRF4, IL‐9, and Th9 cells in the CD4(+) T cells of SLE patients and healthy volunteers. In addition, Bach2 overexpression inhibited the levels of IL‐9 and Th9 cells, whereas IRF4 upregulation enhanced the levels of IRF4 and IL‐9 and Th9 cells in the CD4(+) T cells of SLE patients and healthy volunteers. The effect of IRF4 up‐regulation was abolished by Bach2 overexpression. In summary, our work suggests that Bach2 overexpression represses Th9 cell differentiation by suppressing IRF4 expression in SLE, and thus, Bach2 may be a novel potential target for SLE treatment. |
format | Online Article Text |
id | pubmed-7876501 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-78765012021-02-18 Bach2 overexpression represses Th9 cell differentiation by suppressing IRF4 expression in systemic lupus erythematosus Sheng, Yujun Zhang, Jiali Li, Keke Wang, Hongyan Wang, Wenjun Wen, Leilei Gao, Jinping Tang, Xianfa Tang, Huayang Huang, He Cai, Minglong Yuan, Tao Liu, Lu Zheng, Xiaodong Zhu, Zhengwei Cui, Yong FEBS Open Bio Research Articles Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by abnormal activation of T cells and caused by an imbalance in the production and clearance of apoptotic cells. We previously showed that the transcription regulator Bach2 regulated abnormal B‐cell activation in SLE. Here, we investigated whether Bach2 was also involved in Th9 cell differentiation in SLE. We found that the proportion of Th9 cells was enhanced in the peripheral blood mononuclear cells (PBMC) of SLE patients. The PBMC and CD4(+) T cells of SLE patients exhibited a decrease of Bach2 expression and an increase of IL‐9 expression. Furthermore, Bach2 overexpression significantly repressed the levels of PU.1, IRF4, IL‐9, and Th9 cells in the CD4(+) T cells of SLE patients and healthy volunteers. In addition, Bach2 overexpression inhibited the levels of IL‐9 and Th9 cells, whereas IRF4 upregulation enhanced the levels of IRF4 and IL‐9 and Th9 cells in the CD4(+) T cells of SLE patients and healthy volunteers. The effect of IRF4 up‐regulation was abolished by Bach2 overexpression. In summary, our work suggests that Bach2 overexpression represses Th9 cell differentiation by suppressing IRF4 expression in SLE, and thus, Bach2 may be a novel potential target for SLE treatment. John Wiley and Sons Inc. 2020-12-22 /pmc/articles/PMC7876501/ /pubmed/33249782 http://dx.doi.org/10.1002/2211-5463.13050 Text en © 2020 The Authors. FEBS Open Bio published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Articles Sheng, Yujun Zhang, Jiali Li, Keke Wang, Hongyan Wang, Wenjun Wen, Leilei Gao, Jinping Tang, Xianfa Tang, Huayang Huang, He Cai, Minglong Yuan, Tao Liu, Lu Zheng, Xiaodong Zhu, Zhengwei Cui, Yong Bach2 overexpression represses Th9 cell differentiation by suppressing IRF4 expression in systemic lupus erythematosus |
title | Bach2 overexpression represses Th9 cell differentiation by suppressing IRF4 expression in systemic lupus erythematosus |
title_full | Bach2 overexpression represses Th9 cell differentiation by suppressing IRF4 expression in systemic lupus erythematosus |
title_fullStr | Bach2 overexpression represses Th9 cell differentiation by suppressing IRF4 expression in systemic lupus erythematosus |
title_full_unstemmed | Bach2 overexpression represses Th9 cell differentiation by suppressing IRF4 expression in systemic lupus erythematosus |
title_short | Bach2 overexpression represses Th9 cell differentiation by suppressing IRF4 expression in systemic lupus erythematosus |
title_sort | bach2 overexpression represses th9 cell differentiation by suppressing irf4 expression in systemic lupus erythematosus |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7876501/ https://www.ncbi.nlm.nih.gov/pubmed/33249782 http://dx.doi.org/10.1002/2211-5463.13050 |
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