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Rheumatoid arthritis (RA) is a chronic disease of connective tissue caused by intolerance to self-antigens. Regulatory T cells (Tregs) are key players in maintaining autotolerance through a variety of suppressor mechanisms. RA is generally believed to develop due to disorders in Tregs; however, there is no consensus on this issue. Thus, the present study focused on phenotypical analysis of Treg cells and their ability to suppress CD4+ and CD8+ cell proliferation. The present study used peripheral blood samples from 21 patients with RA and 22 healthy donors. The CD25+FoxP3+ subpopulation of Tregs was analyzed using flow cytometry to evaluate the expression of CTLA-4, PD-L1, HLA-DR, CCR4, CD86 and RORyt. Tregs suppressor activity was calculated in terms of suppression of the proliferation of CD4+ and CD8+ lymphocytes in vitro. Suppressor activity of the total Treg population did not differ between patients with RA and healthy donors. However, the patients had elevated CD25loFoxP3+ levels and lower CD25hiFoxP3+ levels; in addition, they had more activated Tregs expressing PD-L1, HLA-DR, CCR4 and CD86. The surface expression of CTLA-4 was below the reference level. The patients also had transitional FoxP3+RORyt+ cells and elevated CD4+RORyt+ levels, which were highly correlated with disease activity. These results show that in RA, Treg cells are activated and have an immunosuppressive activity. However, it is the transitional FoxP3+RORyt+ cells and increased CD4+RORyt+ percentages in peripheral blood that appear to be associated with the pathological conversion of some Treg cells into Th-17. This process appears to be key in RA pathogenesis.

T‑regulatory cells from patients with rheumatoid arthritis retain suppressor functions in vitro