編碼轉(zhuǎn)錄因子BACH2的一個(gè)位點(diǎn)內(nèi)的多態(tài)性，與包括哮喘,、多發(fā)性硬化,、克羅恩氏病、腹腔病和1-型糖尿病在內(nèi)的若干種過(guò)敏和自體免疫疾病相關(guān),。這篇論文識(shí)別出了BACH2可能用來(lái)幫助自體免疫的一個(gè)機(jī)制,。Roychoudhuri等人解釋了BACH2是怎樣通過(guò)穩(wěn)定調(diào)控性T-細(xì)胞的分化來(lái)抑制其他細(xì)胞命運(yùn)從而限制自體免疫的。這些發(fā)現(xiàn)說(shuō)明,，BACH2起CD4+ T-細(xì)胞分化的一個(gè)調(diào)控因子的作用,，通過(guò)控制耐受與免疫之間的平衡來(lái)防止炎癥,。（生物谷Bioon.com）
生物谷推薦英文摘要：
Nature doi:10.1038/nature12199
BACH2 represses effector programs to stabilize Treg-mediated immune homeostasis
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 et al.
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 activation that stabilizes immunoregulatory capacity while repressing the differentiation programs of multiple effector lineages in CD4+ T cells. BACH2 was required for efficient formation of regulatory (Treg) cells and consequently for suppression of lethal inflammation in a manner that was Treg-cell-dependent. Assessment of the genome-wide function of BACH2, however, revealed that it represses genes associated with effector cell differentiation. Consequently, its absence during Treg polarization resulted in inappropriate diversion to effector lineages. In addition, BACH2 constrained full effector differentiation within TH1, TH2 and TH17 cell lineages. These findings identify BACH2 as a key regulator of CD4+ T-cell differentiation that prevents inflammatory disease by controlling the balance between tolerance and immunity.
