We investigated monocyte-mediated suppression of T lymphocyte blastogenesis in normals and patients with systemic lupus erythematosus (SLE). When monocytes from normals were cocultured with auto-logous T lymphocytes with a ratio of 1:1 and stimulated with phytohemagglutinin (PHA), 3H-thymidine incorporation by T lymphocytes was suppressed. This monocyte-mediated suppression was reversed by purine nucleoside phosphorylase substrate, deoxyguanosine. In SLE patients, both monocyte-mediated suppression and its reversal by deoxyguanosine were defective. The defective function was observed both in patients with active and inactive diseases. The defective function was studied sequentially before and after change in the clinical status of patients. The defects remained unaffected regardless of the disease activity. The defects in monocyte-mediated suppression and its reversal by deoxyguanosine in SLE patients as demonstrated in our study suggest the presence of intrinsic monocyte dysfunction in SLE.

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