CD4+ CD52lo T-cell expression contributes to the development of systemic lupus erythematosus.

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K19604
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Collagenous pathology/Allergology
• Research Institution: Nagasaki University
• Principal Investigator: UMEDA Masataka 長崎大学, 病院(医学系), 助教 (20750053)
• Research Collaborator: KOGA Tomohiro 長崎大学, 医歯薬学総合研究科(医学系), 助教 (90537284) ; ICHINOSE Kunihiro 長崎大学, 医歯薬学総合研究科(医学系), 講師 (60437895)
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: 全身性エリテマトーデス / CD52 / T細胞

Outline of Final Research Achievements

The CD52 is widely expressed in lymphocytes. CD4+CD52hi T cells are functioning suppressor CD4+T cells. We investigated the role of the immune regulation of CD4+CD52 T cells in systemic lupus erythematosus (SLE). CD4+CD52lo T cells were increased in SLE patients, in positive correlation with SLEDAI, anti-ds-DNA antibody, and IgG concentration. Circulating follicular helper-like T cells (Tfh-like cells) were also increased in SLE, in positive correlation with CD4+CD52lo T cells. Chemokine receptor 8 (CCR8) expression in CD4+CD52lo T cells was increased. In vitro experiments using CD4 T cells of SLE patients showed that thymus and activation-regulated chemokine (TARC), a ligand of CCR8, contributed to the development of CD4+CD52hi T cells into CD4+CD52lo T cells. Our findings suggest that CD4+CD52lo T-cell upregulation is involved in the production of pathogens by autoantibodies, and TARC may contribute to the development of SLE through an aberrant induction of CD4+CD52lo T cells.

Free Research Field

リウマチ・膠原病内科学分野