EAF2 mediates germinal centre B-cell apoptosis to suppress excessive immune responses and prevent autoimmunity
EAF2 has been previously known as a transcriptional elongation factor and a proapoptotic gene lost in prostate cancer. Here the authors show that EAF2 is required for apoptosis of germinal centre B cells, and that EAF2-deficient mice develop excessive antibody responses and autoimmunity.
Main Authors: | , , , , , , , , |
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Format: | Article |
Language: | English |
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Nature Portfolio
2016-03-01
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Series: | Nature Communications |
Online Access: | https://doi.org/10.1038/ncomms10836 |
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author | Yingqian Li Yoshimasa Takahashi Shin-ichiro Fujii Yang Zhou Rongjian Hong Akari Suzuki Takeshi Tsubata Koji Hase Ji-Yang Wang |
author_facet | Yingqian Li Yoshimasa Takahashi Shin-ichiro Fujii Yang Zhou Rongjian Hong Akari Suzuki Takeshi Tsubata Koji Hase Ji-Yang Wang |
author_sort | Yingqian Li |
collection | DOAJ |
description | EAF2 has been previously known as a transcriptional elongation factor and a proapoptotic gene lost in prostate cancer. Here the authors show that EAF2 is required for apoptosis of germinal centre B cells, and that EAF2-deficient mice develop excessive antibody responses and autoimmunity. |
first_indexed | 2024-12-20T16:43:23Z |
format | Article |
id | doaj.art-01bd65f796e8492f932b77a49da26010 |
institution | Directory Open Access Journal |
issn | 2041-1723 |
language | English |
last_indexed | 2024-12-20T16:43:23Z |
publishDate | 2016-03-01 |
publisher | Nature Portfolio |
record_format | Article |
series | Nature Communications |
spelling | doaj.art-01bd65f796e8492f932b77a49da260102022-12-21T19:32:59ZengNature PortfolioNature Communications2041-17232016-03-017111310.1038/ncomms10836EAF2 mediates germinal centre B-cell apoptosis to suppress excessive immune responses and prevent autoimmunityYingqian Li0Yoshimasa Takahashi1Shin-ichiro Fujii2Yang Zhou3Rongjian Hong4Akari Suzuki5Takeshi Tsubata6Koji Hase7Ji-Yang Wang8Department of Immunology, School of Basic Medical Sciences, Fudan UniversityDepartment of Immunology, National Institute of Infectious DiseasesLaboratory for Immunotherapy, Center for Integrative Medical Sciences, RIKENDepartment of Immunology, School of Basic Medical Sciences, Fudan UniversityDepartment of Immunology, School of Basic Medical Sciences, Fudan UniversityLaboratory for Autoimmune Diseases, Center for Integrative Medical Sciences, RIKENDepartment of Immunology, Medical Research Institute, Tokyo Medical and Dental UniversityDivision of Mucosal Barriology, International Research and Development Center for Mucosal Vaccines, The Institute of Medical Science, The University of TokyoDepartment of Immunology, School of Basic Medical Sciences, Fudan UniversityEAF2 has been previously known as a transcriptional elongation factor and a proapoptotic gene lost in prostate cancer. Here the authors show that EAF2 is required for apoptosis of germinal centre B cells, and that EAF2-deficient mice develop excessive antibody responses and autoimmunity.https://doi.org/10.1038/ncomms10836 |
spellingShingle | Yingqian Li Yoshimasa Takahashi Shin-ichiro Fujii Yang Zhou Rongjian Hong Akari Suzuki Takeshi Tsubata Koji Hase Ji-Yang Wang EAF2 mediates germinal centre B-cell apoptosis to suppress excessive immune responses and prevent autoimmunity Nature Communications |
title | EAF2 mediates germinal centre B-cell apoptosis to suppress excessive immune responses and prevent autoimmunity |
title_full | EAF2 mediates germinal centre B-cell apoptosis to suppress excessive immune responses and prevent autoimmunity |
title_fullStr | EAF2 mediates germinal centre B-cell apoptosis to suppress excessive immune responses and prevent autoimmunity |
title_full_unstemmed | EAF2 mediates germinal centre B-cell apoptosis to suppress excessive immune responses and prevent autoimmunity |
title_short | EAF2 mediates germinal centre B-cell apoptosis to suppress excessive immune responses and prevent autoimmunity |
title_sort | eaf2 mediates germinal centre b cell apoptosis to suppress excessive immune responses and prevent autoimmunity |
url | https://doi.org/10.1038/ncomms10836 |
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