作者
Rahul Roychoudhuri, Kiyoshi Hirahara, Kambiz Mousavi, David Clever, Christopher A Klebanoff, Michael Bonelli, Giuseppe Sciumè, Hossein Zare, Golnaz Vahedi, Barbara Dema, Zhiya Yu, Hui Liu, Hayato Takahashi, Mahadev Rao, Pawel Muranski, Joseph G Crompton, George Punkosdy, Davide Bedognetti, Ena Wang, Victoria Hoffmann, Juan Rivera, Francesco M Marincola, Atsushi Nakamura, Vittorio Sartorelli, Yuka Kanno, Luca Gattinoni, Akihiko Muto, Kazuhiko Igarashi, John J O’Shea, Nicholas P Restifo
发表日期
2013/6/27
期刊
Nature
卷号
498
期号
7455
页码范围
506-510
出版商
Nature Publishing Group UK
简介
Through their functional diversification, distinct lineages of CD4+ T cells can act to either drive or constrain immune-mediated pathology. Transcription factors are critical in the generation of cellular diversity, and negative regulators antagonistic to alternate fates often act in conjunction with positive regulators to stabilize lineage commitment. Genetic polymorphisms within a single locus encoding the transcription factor BACH2 are associated with numerous autoimmune and allergic diseases including asthma, Crohn’s disease,, coeliac disease, vitiligo, multiple sclerosis and type 1 diabetes. Although these associations point to a shared mechanism underlying susceptibility to diverse immune-mediated diseases, a function for BACH2 in the maintenance of immune homeostasis has not been established. Here, by studying mice in which the Bach2 gene is disrupted, we define BACH2 as a broad regulator of immune …
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