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NLRC 3 expression in dendritic cells attenuates CD 4 + T cell response and autoimmunity
Author(s) -
Fu Yuling,
Zhan Xiaoxia,
Wang Yichong,
Jiang Xiaobing,
Liu Min,
Yang Yalong,
Huang Yulan,
Du Xialin,
Zhong XiaoPing,
Li Laisheng,
Ma Li,
Hu Shengfeng
Publication year - 2019
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.15252/embj.2018101397
Subject(s) - biology , autoimmunity , microbiology and biotechnology , dendritic cell , cell , antigen , immune system , immunology , biochemistry
NOD ‐like receptor ( NLR ) family CARD domain containing 3 ( NLRC 3), an intracellular member of NLR family, is a negative regulator of inflammatory signaling pathways in innate and adaptive immune cells. Previous reports have shown that NLRC 3 is expressed in dendritic cells ( DC s). However, the role of NLRC 3 in DC activation and immunogenicity is unclear. In the present study, we find that NLRC 3 attenuates the antigen‐presenting function of DC s and their ability to activate and polarize CD 4 + T cells into Th1 and Th17 subsets. Loss of NLRC 3 promotes pathogenic Th1 and Th17 responses and enhanced experimental autoimmune encephalomyelitis ( EAE ) development. NLRC 3 negatively regulates the antigen‐presenting function of DC s via p38 signaling pathway. Vaccination with NLRC 3‐overexpressed DC s reduces EAE progression. Our findings support that NLRC 3 serves as a potential target for treating adaptive immune responses driving multiple sclerosis and other autoimmune disorders.