| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Outline of Final Research Achievements |
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by autoantibody production and associated with a wide range of clinical manifestations. Early growth response gene-2 (EGR2), a zinc-finger transcription factor, is known to affect susceptibility to SLE in human. We previously reported CD4+CD25-Foxp3-LAG3+ regulatory T cells (LAG3 Tregs) that characteristically express Egr2. In this study, we revealed that LAG3 Tregs, but not CD4+CD25+ Tregs, produce enormous amounts of TGF-β3 in an Egr2-dependent manner. TGF-β3 effectively suppressed autoantibody production from B cells through suppression of Syk, STAT6, and NF-κB pathways. Intriguingly, Egr3 was able to compensate the function of Egr2. These findings elucidated the mechanisms of T cell anergy-associated gene Egr2-mediated regulation of humoral immunity.
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