This study was undertaken to delineate the nature of the immunoregulatory defect in patients with systemic lupus erythematosus (SLE). Thirty-eight SLE patients were studied and it was found that in addition to an absolute T lymphocytopenia, these patients had a selective proportional and quantitative deficiency (P < 0.01) of a subpopulation of T cells possessing a receptor for IgG (TG). This T cell subpopulation has been previously demonstrated to be the suppressor cell population in pokeweed mitogen (PWM)-driven intracytoplasmic Ig production. T cells with a receptor for IgM (TM) which have been shown to be the helper T cells for Ig production were not significantly different from normals in proportion or absolute numbers.
By employing a PWM-induced plaque-forming cell (PFC) assay against sheep red blood cells (SRBC), it was shown that SLE patients had a markedly reduced response of 18 (±4.2) PFC/106 lymphocytes compared to normals with 153 (±18.4) PFC/106 lymphocytes (P < 0.001). This suppressed PFC response was felt to result from in vivo polyclonal activation associated with the autoimmune state.
SLE patients had a marked defect in the ability of their lymphocytes after Con A activation to generate suppressor cells of the PWM-induced PFC response, whereas their ability to be suppressed by suppressor stimuli appeared intact. Despite considerable variability from patient to patient, lymphocytes from SLE patients in general had adequate T helper cell function and could be helped by normal allogeneic T helper cells. Thus, this study demonstrates that SLE patients have a quantitative defect in a subpopulation of T cells with suppressor capability. In addition, they have a defect in the ability to generate suppressor cell function upon appropriate activation. These findings may lend further insight into the understanding of the immunoregulatory defect in SLE.