title: Emerging roles of Egr2 and Egr3 in the control of systemic autoimmunity.
abstract: 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-β1. 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.
authors.affiliation: Department of Allergy and Rheumatology, Graduate School of Medicine.
authors.forename: Kaoru
authors.initials: K
authors.lastname: Morita
authors.affiliation: Department of Allergy and Rheumatology, Graduate School of Medicine.|Max Planck-University of Tokyo Center for Integrative Inflammology, University of Tokyo, Tokyo, Japan.
authors.forename: Tomohisa
authors.initials: T
authors.lastname: Okamura
authors.affiliation: Department of Allergy and Rheumatology, Graduate School of Medicine.
authors.forename: Shuji
authors.initials: S
authors.lastname: Sumitomo
authors.affiliation: Department of Allergy and Rheumatology, Graduate School of Medicine.
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Iwasaki
authors.affiliation: Department of Allergy and Rheumatology, Graduate School of Medicine kfujio-tky@umin.ac.jp.
authors.forename: Keishi
authors.initials: K
authors.lastname: Fujio
authors.affiliation: Department of Allergy and Rheumatology, Graduate School of Medicine.
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Yamamoto
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology; D015551:Autoimmunity / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D051767:Early Growth Response Protein 2 / Q000235:genetics / Q000276:immunology*; D051776:Early Growth Response Protein 3 / Q000235:genetics / Q000276:immunology*; D006801:Humans; D016753:Interleukin-10 / Q000276:immunology; D020381:Interleukin-17 / Q000276:immunology; D008180:Lupus Erythematosus, Systemic / Q000235:genetics / Q000276:immunology*; D051379:Mice; D013601:T-Lymphocytes / Q000276:immunology; D016212:Transforming Growth Factor beta / Q000276:immunology
chemical_list: D051767:Early Growth Response Protein 2; D020381:Interleukin-17; D016212:Transforming Growth Factor beta; D016753:Interleukin-10; D051776:Early Growth Response Protein 3
keywords: CD4+ T cells; Egr2; Egr3; IL-10; IL-17; LAG3; TGF-β1; Th17; Treg; systemic lupus erythematosus