Vicious circle: systemic autoreactivity in Ro52/TRIM21-deficient mice

被引:28
作者
Bolland, Silvia [1 ]
Garcia-Sastre, Adolfo [2 ]
机构
[1] NIAID, NIH, Immunogenet Lab, Rockville, MD 20852 USA
[2] Mt Sinai Sch Med, Pathogens Inst, New York, NY 10029 USA
关键词
AICARDI-GOUTIERES-SYNDROME; INTERFERON-INDUCIBLE GENE; LUPUS-ERYTHEMATOSUS; I INTERFERON; DENDRITIC CELLS; CYTOKINE EXPRESSION; SJOGRENS-SYNDROME; FAMILY PROTEINS; UP-REGULATION; IFN-ALPHA;
D O I
10.1084/jem.20091507
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Dysregulated innate responses, particularly excessive activation of interferon (IFN) pathways, have been implicated in the development of autoimmune pathologies. Autoreactivity frequently targets IFN-inducible genes such as the Ro autoantigens, which ubiquitinate and inhibit interferon regulatory factors (IRFs). A new study validates the role of these common autoantigens in preventing autoimmunity. The findings reveal that injury-induced systemic autoimmune disease is exacerbated in the absence of Ro52/Trim21 and is driven by the IL-23-Th17 pathway.
引用
收藏
页码:1647 / 1651
页数:5
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