Abstract
Peripheral blood lymphocytes from 20 patients with systemic lupus erythematosus (SLE) were defective in their ability to secrete immunoglobulin M (IgM) in a pokeweed mitogen (PWM)-stimulated in vitro culture system. To characterize this abnormality, the mononuclear cells were separated into three functional subpopulations: (i) bone marrow-derived (B) cells which secrete immunoglobulin; (ii) a thymus-derived (T) lymphocyte fraction; and (iii) an irradiated T-cell fraction with predominant helper function. Coculture experiments with subsequent radioimmunoassay of the quantity of immunoglobulin secreted allowed comparisons of the immunoregulatory functions of the SLE-helper T, SLE suppressor T, and SLE B cells with functions of control lymphocyte fractions. The major defect defined was an inability of the SLE B cell to secrete normal amounts of IgM. This was not due to suppression by monocytes since the removal of phagocytic cells and the addition of separated monocytes to the cultures demonstrated generation of normal helper signals by SLE monocytes. Nor were inadequate numbers of IgM secreting B cells available since limiting dilution studies showed a normal precursor frequency of PWM-stimulatable, IgM secreting SLE B cells. SLE T cells showed a normal helper effect on the secretion of IgM by control B cells. Thus, these in vitro coculture studies designate a primary immunologic defect in SLE to the B cell and not in the suppressor or helper functions of the T cell.
Published Version
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