Journal
RHEUMATOLOGY
Volume 55, Issue -, Pages 76-81Publisher
OXFORD UNIV PRESS
DOI: 10.1093/rheumatology/kew342
Keywords
systemic lupus erythematosus; Egr2; Egr3; CD4(+) T cells; Th17; Treg; LAG3; TGF-beta 1; IL-10; IL-17
Categories
Funding
- Ministry of Health, Labour and Welfare, Ministry of Education, Culture, Sports, Science and Technology KAKENHI [23229007, 24390252, 25461493, 16K09918]
- Cell Science Research Foundation
- Grants-in-Aid for Scientific Research [16K09918, 24390252, 16K15510, 23229007, 25461493, 15K19566] Funding Source: KAKEN
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SLE is an autoimmune disease characterized by multiple organ damage mediated by autoantibodies and autoreactive T cells. Approaches utilizing genetically engineered mice as well as genome-wide association studies have identified a number of lupus-related genes. Recently, early growth response gene 2 (Egr2) and Egr3 have emerged as regulatory molecules that suppress excessive immune responses. Mice deficient for Egr2 and Egr3 develop a lupus-like disease with dysregulated activation of effector T cells. Furthermore, Egr2 and Egr3 confer suppressive activity to CD4(+) T cells and regulate the production of inhibitory cytokines such as IL-10 and TGF-beta 1. These findings may have implications for a wide range of immune-related pathologies and suggest the possibility that efforts exploiting Egr2 and Egr3 could aid in the development of therapeutic applications. This review summarizes the recent advances regarding the roles of Egr2 and Egr3 on T cells in the control of autoimmunity.
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