PRODUCTION OF A SUPPRESSOR FACTOR BY HUMAN ADHERENT CELLS TREATED WITH MYCOBACTERIUM-TUBERCULOSIS - ABSENCE IN SYSTEMIC LUPUS-ERYTHEMATOSUS

  • 1 January 1981
    • journal article
    • research article
    • Vol. 46  (1) , 82-88
Abstract
When human peripheral blood mononuclear cells are activated by mitogens in the presence of M. tuberculosis, considerable suppression of 3H-thymidine incorporation is observed. Proliferation of mononuclear cells from patients with SLE [systemic lupus erythematosus] was not suppressed by treatment with mycobacteria. Analysis of the 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. 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 maneuvers restored the ability of SLE adherent cells to produce suppressor factor. Normal adherent cells continued to produce the factor after prior treatment with varying concentrations of human serum albumin-anti-human serum albumin complexes. A basic adherent cell defect probably exists in SLE; under certain circumstances this may give rise to a secondary defect of suppressor cell activation.