[Changes and clinical significance of peripheral blood CD8(+)CD25(+)T cells in rheumatoid arthritis patients]
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1Department of Rheumatology and Immunology, the Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou 450002, China.
Abstract:
Objective: To investigate the expression of CD8(+)CD25(+)T cells in peripheral blood of patients with rheumatoid arthritis (RA) and its correlation with clinical indicators of rheumatoid arthritis. Methods: Peripheral blood was collected from 38 patients with RA, and 20 healthy control subjects, RA patients admitted to Peking University people's hospital from May to October 2018, and record the RA patients with the clinical manifestations and laboratory indexes, extraction in the peripheral blood lymphocytes, using flow cytometry to analyse the percentage of CD8(+)CD25(+)T cells in peripheral blood, by using the software SPASS20 and Prism6 to analyze its correlation with clinical and laboratory indices. Results: The expression of CD8(+)CD25(+)T cells in peripheral blood of RA patients was significantly increased, which was statistically different from that of healthy patients (P<0.05). CD8(+)CD25(+)T cells in peripheral blood of RA patients showed significant positive correlation with ESR(r=0.352,P=0.030), CCP(r=0.312,P=0.047) and DAS28(r=0.330,P=0.043), and negatively correlated with C3 (r=-0.354,P=0.046) and C4(r=-0.440,P=0.010).No significant correlation was found in other indicators. In RA patients, there were statistically significant differences in CD8(+)CD25(+)T cells between the low-disease active group and the high-disease active group(P<0.05), but CD8(+)CD25(+)T cells between the low-disease active group and the moderate-disease active group, or between the moderate-disease active group and the high-disease active group had no significant statistical difference. Conclusion: CD8(+)CD25(+)Tcells in peripheral blood of patients with RA are significantlyincreased, and aresignificantly correlated with laboratory and clinical indicators, which may play an important role in the pathogenesis of rheumatoid arthritis.
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