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Capicua deficiency induces autoimmunity and promotes follicular helper T cell differentiation via derepression of ETV5
- Capicua deficiency induces autoimmunity and promotes follicular helper T cell differentiation via derepression of ETV5
- Park, Sungjun; Lee, Seungwon; Lee, Choong-Gu; Park, Guk Yeol; Hong, Hyebeen; Lee, Jeon-Soo; Kim, Young Min; Lee, Sung Bae; Hwang, Daehee; Choi, Youn Soo; Fryer, John D.; Im, Sin-Hyeog; Lee, Seung-Woo; Lee, Yoontae
- DGIST Authors
- Lee, Sung Bae; Hwang, Daehee
- Issue Date
- Nature Communications, 8
- Article Type
- C MAF; Center B Cell; ETS Transcription Factors; Expression; Family; Germinal Center Response; In Vivo; Interferon Gamma; Repressor Capicua; Transgenic Mice
- High-affinity antibody production through the germinal centre (GC) response is a pivotal process in adaptive immunity. Abnormal development of follicular helper T (T(FH)) cells can induce the GC response to self-antigens, subsequently leading to autoimmunity. Here we show the transcriptional repressor Capicua/CIC maintains peripheral immune tolerance by suppressing aberrant activation of adaptive immunity. CIC deficiency induces excessive development of T(FH) cells and GC responses in a T-cell-intrinsic manner. ETV5 expression is derepressed in Cic null T(FH) cells and knockdown of Etv5 suppresses the enhanced T(FH) cell differentiation in Cic-deficient CD4+ T cells, suggesting that Etv5 is a critical CIC target gene in T(FH) cell differentiation. Furthermore, we identify Maf as a downstream target of the CIC-ETV5 axis in this process. These data demonstrate that CIC maintains T-cell homeostasis and negatively regulates T(FH) cell development and autoimmunity. © The Author(s) 2017.
- Nature Publishing Group
- Related Researcher
Lee, Sung Bae
SB LAB(Lab of Neurodegenerative diseases and Aging)
Cellular mechanism of neurodegenerative diseases; Neuronal maintenance and remodeling; 퇴행성 뇌질환의 세포기전; 신경계 유지 및 리모델링 연구
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