Relationship between systemic lupus erythematosus T cell subsets, anti-T cell antibodies, and T cell functions.

Abstract

Previous studies have shown that patients with systemic lupus erythematosus (SLE) had differing T cell T4+/T8+ ratios and that the ratio correlated with clinical features of the disease. In the present study, we wished to determine whether the peripheral blood T cell subsets in these patients were related to the specificity of anti-T cell antibodies found in their plasma. Plasma from 24 SLE patients that reacted with greater than 20% of normal T cells were analyzed for their effect on in vitro pokeweed mitogen-stimulated immunoglobulin synthesis and for their reactivity with human T4+ and T8+ cells. Anti-T cell antibodies found in SLE patients have a spectrum of reactivities. We concentrated upon antibodies that interfere with suppressor function. One group of SLE anti-T cell antibodies reacts preferentially with the T8+ suppressor effector cell whereas another is reactive with T4+ suppressor inducer subsets. SLE patients with high T4+/T8+ ratios had anti-T cell antibodies predominantly reactive with the T8+ suppressor effector cells. Patients with low T4+/T8+ ratios, on the other hand, had anti-T cell antibodies reactive with either the T4+ suppressor inducer or with both the T4+ suppressor inducer and T8+ suppressor effector cells. In addition, a fourth group was defined whose anti-T cell antibodies were neither reactive with a functional T4+ suppressor inducer nor a functional T8+ suppressor effector cells. There was a significant correlation between the circulating T4+/T8+ ratio of peripheral T cells in these patients and the relative ability of their anti-T cell antibodies to kill T8+ cells vs. T4+ cells (gamma = 0.666, P less than 0.001). These results support the notion that in SLE different cellular defects in the immunoregulatory circuit underlie the development of autoimmune reactions and that the anti-T cell antibodies may cause numerical and functional deficiencies in T cell subsets.