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Abstract 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.
Fauci et al. (Sun,) studied this question.