摘要
We sought to investigate the expression of Fas and FasL on T cell surface and caspase 8 involvement in T cell apoptosis promoted by serum IL-10 in systemic lupus erythematosus （SLE） patients. Cells and sera were obtained from 35 SLE patients. Apoptosis of T cells in patients with SLE was increased and associated with the SLE disease activity index （SLEDAI）. Elevated expression of Fas and FasL on T cell surface contributed to increased apoptosis of T cells. Increased IL-10 in the sera of SLE patients was capable of inducing Fas and FasL expression on CD4^＋T cell surface, promoting apoptosis of this cell subset. Decreased IL-10 serum levels and low expression of Fas were found in 5 patients of the first follow-up group after 2-month treatment. In another group with one-year treatment, the SLEDAI declined to inactive scores. Serum IL-10 was decreased significantly, and expression of Fas and FasL on T cells was also reduced. Declined apoptosis was predominant only in CD4^＋T cell subset. When sera with high level of IL-10 were used to culture PBMCs from healthy controls, activated caspase 8 was elevated in CD3^＋T, CD4^＋T and CD8^＋T cells. The study showed that serum IL-10 induced apoptosis of T cell subsets via the caspase 8 pathway initiated by Fas signaling. Increased apoptosis of T cells contributes to autoantigen burden, which is pathogenic in the development of SLE.
We sought to investigate the expression of Fas and FasL on T cell surface and caspase 8 involvement in T cell apoptosis promoted by serum IL-10 in systemic lupus erythematosus （SLE） patients. Cells and sera were obtained from 35 SLE patients. Apoptosis of T cells in patients with SLE was increased and associated with the SLE disease activity index （SLEDAI）. Elevated expression of Fas and FasL on T cell surface contributed to increased apoptosis of T cells. Increased IL-10 in the sera of SLE patients was capable of inducing Fas and FasL expression on CD4^＋T cell surface, promoting apoptosis of this cell subset. Decreased IL-10 serum levels and low expression of Fas were found in 5 patients of the first follow-up group after 2-month treatment. In another group with one-year treatment, the SLEDAI declined to inactive scores. Serum IL-10 was decreased significantly, and expression of Fas and FasL on T cells was also reduced. Declined apoptosis was predominant only in CD4^＋T cell subset. When sera with high level of IL-10 were used to culture PBMCs from healthy controls, activated caspase 8 was elevated in CD3^＋T, CD4^＋T and CD8^＋T cells. The study showed that serum IL-10 induced apoptosis of T cell subsets via the caspase 8 pathway initiated by Fas signaling. Increased apoptosis of T cells contributes to autoantigen burden, which is pathogenic in the development of SLE.
