[Impaired apoptosis of peripheral blood CD4+T cells in patients with rheumatoid arthritis].

OBJECTIVE

To investigate the role of CD4+T cell apoptosis in the pathogenesis of rheumatoid arthritis (RA).

METHODS

The study enrolled 30 RA cases and 12 normal individuals as subjects. The apoptosis level of CD4+T lymphocytes in the patients with RA and the control individuals were measured by annexin V-FITC/PI staining combined with flow cytometry. The expression levels of Fas, FasL, caspase-8, caspase-3, Bcl-2 and Bax mRNAs were detected using real-time quantitative PCR (qRT-PCR); the expressions of Fas, FasL, caspase-8, caspase-3 proteins were observed using Western blotting. The correlations between the expressions of the apoptosis-related proteins and the clinical activity parameters were analyzed.

RESULTS

The apoptosis level of CD4+T lymphocytes in RA patients was significantly lower than that in the healthy controls, and it was negatively correlated with erythrocyte sedimentation rate (ESR) and rheumatoid factor (RF). Compared with the healthy control group, the expression levels of Fas, FasL, caspase-8, caspase-3 and Bax mRNAs in CD4+T cells of the RA patients were significantly reduced, whereas Bcl-2 mRNA was significantly elevated. The expression of Fas mRNA in CD4+T cells was negatively correlated with traditional Chinese medicine symptom score, whereas Bcl-2 mRNA was positively correlated with cyclic citrullinated peptide (CCP). Compared with the control group, the expressions of Fas, FasL, caspase-8 and caspase-3 proteins in CD4+T cells in the RA patients significantly decreased. The expression level of Fas protein was positively correlated with C-reactive protein (CRP), whereas FasL was negatively correlated with the time of morning stiffness.

CONCLUSION

There is a decrease in the apoptosis of peripheral blood CD4+T cells in patients with RA, which has been found related to the decreased expressions of the apoptosis-related proteins (Fas, FasL, caspase-8, caspase-3, Bax) and the increased expression of Bcl-2. The study suggests that Fas-mediated apoptosis plays a role in the development of RA.