The transcription factor RelB restrains group 2 innate lymphoid cells and type 2 immune pathology in vivo  

作　　者：Lei Zhang Yuanlin Ying Shuqiu Chen Preston R.Arnold Fafa Tian Laurie J.Minze Xiang Xiao Xian C.Li 

机构地区：[1]Immunobiology and Transplant Science Center,and Department of Surgery,Houston Methodist Hospital,Texas Medical Center,Houston,Texas,USA [2]Department of Neurology,Xiangya Hospital,Central South University,Changsha,China [3]Department of Urology,Southeast University Zhongda Hospital,Nanjing,China [4]Department of Surgery,Weill Cornell Medical College of Cornell University,New York,NY,USA

出　　处：《Cellular & Molecular Immunology》2021年第1期230-242,共13页中国免疫学杂志（英文版）

基　　金：supported in part by the National Institutes of Health(R01AI080779);the Kleberg Foundation.

摘　　要：The exact relationships between group 2 innate lymphoid cells(ILC2s)and Th2 cells in type 2 pathology,as well as the mechanisms that restrain the responses of these cells,remain poorly defined.Here we examined the roles of ILC2s and Th2 cells in type 2 lung pathology in vivo using germline and conditional fie/b-deficient mice.We found that mice with germline deletion of Relb^(-/-)spontaneously developed prominent type 2 pathology in the lung,which contrasted sharply with mice with T-cell-specific Relb deletion(Relb^(f/f)Cd4-Cre),which were healthy with no observed autoimmune pathology.We also found that in contrast to wild-type B6 mice,Rel6-defident mice showed markedly expanded ILC2s but not ILC1s or ILC3s.Moreover,adoptive transfer of naive CD4^(+)T cells into Rag1^(-/-)Relb^(-/-)hosts induced prominent type 2 lung pathology,which was inhibited by depletion of ILC2s.Mechanistically,we showed that Relb deletion led to enhanced expression of Bcl11b,a key transcription factor for ILC2s.We concluded that RelB plays a critical role in restraining ILC2s,primarily by suppressing Bcl11b activity,and consequently inhibits type 2 lung pathology in vivo.

关 键 词：Allergic inflammation Innate lymphoid cells NF-KB RELB Th2 cells type 2 pathology 

分 类 号：R392[医药卫生—免疫学]