Defective suppressor T-cell activity in systemic lupus erythematosus

Abstract Systemic lupus erythematosus (SLE) is a systemic immunologic disease with a suspected autoimmune etiology. Recent studies in NZB mice have suggested a defect in T-suppressor cells, possibly related to an impairment of thymic hormone secretion, as a basis for autoimmunity. In the present report we analyzed the suppressive potential of lymphocytes from SLE patients. To obtain suppressor T cells, peripheral blood lymphocytes (PBL) from patients and healthy donors were stimulated with concanavalin A (Con A) and then cocultured in a mixed lymphocyte reaction (MLC). The level of suppressor activity mediated by the lectin-activated lymphocytes was not correlated with clinical disease activity, organ-system involvement, drug therapy, and anti-DNA antibodies. Thirty patients with lupus (14–60 years of age) were studied. Seventy percent showed a decrease in T-cell suppressor activity (mean = 37% suppression) as compared to that of controls (mean = 74%). Forty percent of those with abnormal activity showed a profound defect, while 60% showed a milder or partial defect. Of those considered to have inactive disease, mean suppression was 50%; those with active disease had a mean suppression of 34%. Although there was a trend for those with more active disease to show less T-cell suppression, no consistent correlations were noted with organ-system involvement, drug therapy, or DNA binding. No relationship between thymic hormone-factor levels and T-cell suppressive activity was found. Thus, the majority of patients with SLE demonstrate a loss of T-cell suppressor activity in a T-cell assay system, regardless of their disease status. This defect in T-suppressor cells may be important in the pathogenesis of SLE.