Production of a suppressor factor by human adherent cells treated with Mycobacterium tuberculosis: absence in systemic lupus erythematosus.

When human peripheral blood mononuclear cells are activated by mitogens in the presence of Mycobacterium tuberculosis (M. tuberculosis), considerable suppression of 3H-thymidine incorporation is observed. Proliferation of mononuclear cells from patients with SLE was not suppressed by treatment with mycobacteria. Analysis of suppressor effect indicated that normal peripheral blood adherent cells treated with mycobacteria release a soluble factor which activates a precursor cell population to become active suppressor T cells. Although lymphocytes from patients with SLE were responsive to suppressor factor produced by normal adherent cells treated with mycobacteria, SLE adherent cells were incapable of producing suppressor factor when treated in the same way. In order to determine whether the inability of SLE adherent cells to produce suppressor factor was due to the presence of immune complexes on the surface of these cells, SLE adherent cells were trypsinized or preincubated prior to treatment with mycobacteria. Neither of these manoeuvres restored the ability of SLE adherent cells to produce suppressor factor. Furthermore, normal adherent cells continued to produce the factor after prior treatment with varying concentrations of human serum albumin-anti-human serum albumin complexes. The results suggest that a basic adherent cell defect exists in SLE and that under certain circumstances this may give rise to a secondary defect of suppressor cell activation.