CELLULAR IMMUNITY IN SARCOIDOSIS - EVIDENCE FOR AN INTRINSIC DEFECT OF EFFECTOR CELL-FUNCTION

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Abstract
The impaired cellular immunity observed in sarcoidosis may be related to serum inhibitors that exert their effect directly on cells, or indirectly by masking these cells'' surface receptors for mitogens and antigens. To investigate whether the sarcoid lymphocyte abnormality is related to defects at or distal to surface receptors, the binding capacity and affinity for radioiodinated leukoagglutinin of sarcoid lymphocytes and their metabolic responses to the receptor-bound lectin were ascertained in 15 patients and 15 control subjects. Lymphocyte subpopulations were studied with the E[erythrocyte]-rosette and immunofluorescence techniques. Sarcoid lymphocytes possess normal receptor capacity and affinity for radioiodinated leukoagglutinin, but these cells'' metabolic responses to receptor-bound lectin were impaired in all but 4 patients. The patients exhibited T[thymus-derived]-cell lymphopenia, normal B[bone marrow-derived]-cells and an increase in the null cell subpopulation. There was no correlation between the metabolic defect and the presence or magnitude of the T-cell lymphopenia. Serum factors were not excluded as contributors to the immunoincompetence of sarcoidosis. If present, their inhibitory effect is probably not exerted by blocking or masking lymphocyte membrane receptors. Furthermore, there may be an intrinsic defect of effector cell function distal to the plasma membrane receptor site. This defect might precede and lead to T-cell depletion.

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