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Abstract
The immune dysregulation that lead to SLE is complex but has two main characteristics. One is B lymphocyte hyperactivity accompanied by immunoglobulin repertoire changes leading to an increased production of autoantibodies. The other is the impaired cell mediated immunity, which results from both T lymphocyte and antigen- presenting cell abnormalities (Li & Isenberg, 2006).
Interleukin 10 (IL-10) is a pleiotropic cytokine produced by various cell types including T lymphocytes, B lymphocytes, monocytes and mast cells. IL-10 is a potent inducer of B lymphocyte differentiation, as well as inhibitor of helper T cell and antigen presenting cell function. B lymphocyte hyperactivity may result from autocrine and paracrine effects of IL-10 signaling. Some have proposed that the immunologic imbalance in SLE may be related to an abnormally high production of IL-10 (Chun et al., 2007).
The current study included fifty patients suffering from SLE and thirty controls free from any relevant diseases. Both patients and controls were matched by age and sex. All the patients were subjected to disease activity assessment by (M-SLEDAI) index. All subjects were subjected to antinuclear antibodies (ANA) and anti-ds DNA autoantibodies detection using indirect immunofluorescence method. Serum IL-10 level was detected using ELISA. Seeking for the possible mechanism for IL-10 overproduction in SLE, spontaneous production of IL-10 from normal PBMC after exposure to both SLE and control sera was studied using ELISPOT test.
The results showed that SLE patients had higher frequency of ANA autoantibodies as compared to healthy controls. Active SLE patients showed higher titers of anti-ds DNA autoantibodies as compared to inactive SLE patients .A significant correlation was