1. CD4 + CD52 lo T-cell expression contributes to the development of systemic lupus erythematosus.
- Author
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Umeda M, Koga T, Ichinose K, Igawa T, Sato T, Takatani A, Shimizu T, Fukui S, Nishino A, Horai Y, Hirai Y, Kawashiri SY, Iwamoto N, Aramaki T, Tamai M, Nakamura H, Yamamoto K, Abiru N, Origuchi T, Ueki Y, and Kawakami A
- Subjects
- Adolescent, Adult, Antibodies, Antinuclear immunology, Autoantibodies immunology, Case-Control Studies, Female, Humans, Immunoglobulin G immunology, In Vitro Techniques, Male, Middle Aged, Receptors, CCR8 immunology, Severity of Illness Index, Up-Regulation, Young Adult, CD4-Positive T-Lymphocytes immunology, CD52 Antigen immunology, Chemokine CCL17 immunology, Lupus Erythematosus, Systemic immunology
- Abstract
The cell-surface glycoprotein 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., (Copyright © 2017 Elsevier Inc. All rights reserved.)- Published
- 2018
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