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2015 Fiscal Year Final Research Report

An investigation of the role of the transcription repressor Bach2 in CD4 T cell-mediated immune homeostasis

Research Project

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Project/Area Number 25860376
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Immunology
Research InstitutionEhime University

Principal Investigator

Kuwahara Makoto  愛媛大学, 医学部附属病院, その他 (00568214)

Co-Investigator(Renkei-kenkyūsha) Yamashita Masakatsu  愛媛大学, 大学院医学系研究科免疫学, 教授 (00311605)
Project Period (FY) 2013-04-01 – 2016-03-31
KeywordsTh2 / 免疫老化 / Bach2
Outline of Final Research Achievements

The transcriptional repressor Bach2 acts as a key regulator of T cell-mediated immune homeostasis. However, molecular mechanisms by which Bach2 controls T cell-mediated immune homeostasis remain unclear. We found that Bach2 associates with transcriptional factor Batf and binds to the Th2 cytokine gene loci including the Il4 enhancer and locus control regions both of which containing AP-1 motifs, which led to the inhibition of IL-4 production. Furthermore, the spontaneous development of Th2-type lung inflammation and accelerated Th2 cell differentiation caused by the T cell-specific Bach2 deficiency was normalized by the T cell-specific deletion of the Batf gene. These results indicated that Bach2-Batf complex is required to repress the Th2-type immune responses. We also showed that Bach2 inhibits the senescence-associated secretory phenotype (SASP) in senescent CD4 T cells. These findings reveal a critical role of the Bach2 in regulating CD4 T cell-mediated immune homeostasis.

Free Research Field

免疫学

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Published: 2017-05-10  

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