The mechanism of dysregulation of inflammation in systemic lupus erythematosus

2015 Fiscal Year Final Research Report

• Project/Area Number: 25461479
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Collagenous pathology/Allergology
• Research Institution: Yokohama City University
• Principal Investigator: ASAMI Yukiko 横浜市立大学, 医学(系)研究科(研究院), 客員研究員 (40644464)
• Co-Investigator(Kenkyū-buntansha): YOSHIMI Ryusuke 横浜市立大学, 附属病院, 助教 (70585265) ; TAKENO Mitsuhiro 日本医科大学, 医学部, 准教授 (50236494) ; UEDA Atsuhisa 横浜市立大学, 医学部, 准教授 (60295483)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 免疫学 / 内科学 / 膠原病学

Outline of Final Research Achievements

The pathogenesis of systemic lupus erythematosus (SLE) or Sjogren's syndrome (SS) is still unknown. In this study, we investigated the role of autoantigen TRIM21 in SLE pathogenesis. The mRNA level of TRIM21 was higher in peripheral blood mononuclear cells from patients with SLE as compared to healthy controls (HC). TRIM21 mRNA levels correlated positively with SLE disease activity. Type I interferon (IFN) mRNA levels showed a negative correlation with TRIM21 mRNA levels in HC but not in patients with SLE. These results suggest that dysregulation of TRIM21 to function as an negative regulator for type I IFN expression is one of the cause of SLE pathogenesis. Thus TRIM21 may have potential as a therapeutic target for SLE.

Free Research Field

医歯薬学