Significance of increased IL-17-producing Foxp3+ Treg in peripheral blood of patients with active systemic lupus erythematosus
10.3760/cma.j.issn.0254-5101.2019.03.003
- VernacularTitle:活动性系统性红斑狼疮患者外周血IL-17+Foxp3+调节性T细胞升高的意义
- Author:
Zhenjia FAN
1
;
Minghui XUE
;
Lilan JIN
;
Jiafei LIN
;
Gang CAI
Author Information
1. 上海交通大学医学院附属瑞金医院检验科 200025
- Keywords:
Regulatory T cell;
Interleukin-17;
Inflammatory cytokine;
Immunophenotype;
T cell plasticity
- From:Chinese Journal of Microbiology and Immunology
2019;39(3):174-179
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the expression of IL-17-producing regulatory T cells ( Treg) in patients with systemic lupus erythematosus ( SLE) and to analyze their clinical significance. Methods This study recruited 32 patients with SLE ( including 14 with active SLE and 18 with inactive SLE) and 13 healthy subjects matched for age and sex. Flow cytometry was performed to detect the expression of Foxp3 and IL-17 in CD4 T lymphocytes and the phenotypic characteristics of IL-17-producing Treg. Correlations between these cells and clinical indicators of SLE were analyzed. Peripheral CD4+CD25+ T cells were isola-ted from five healthy subjects and then stimulated with IL-6 and IL-1βalone or in combination. An in vitro T cell polarization assay was performed to investigate the role of cytokines in the polarization and regulation of IL-17-producing Treg. Results Compared with the healthy subjects and patients with inactive SLE, the pa-tients with active SLE had a higher percentage of IL-17-producing Treg in peripheral blood. Moreover, the expression of Foxp3 and CD45RA by IL-17-producing Treg in the active SLE group was down-regulated, while that of IL-2, granzyme B (GramB), programmed cell death protein 1 (PD-1) and glucocorticoid-in-duced tumor necrosis factor receptor ( GITR) was up-regulated. Inflammatory cytokines such as IL-6 and IL-1 could induce Treg to produce IL-17. Conclusions This study suggested that increased inflammatory cytokines might correlate with higher percentages of IL-17-producing Treg in patients with active SLE. These cells were a subset of pathogenic Treg failing to prevent autoimmune.
