Interleukin 2 receptors and responsiveness to recombinant human interleukin 2 in patients with systemic lupus erythematosus.

Defects in interleukin 2 (IL2) responsiveness may contribute to immunologic abnormalities in systemic lupus erythematosus (SLE). We studied the acquisition of IL2 receptors and responsiveness to recombinant human IL2 (rIL2) in the peripheral blood mononuclear cells (PBM) of patients with SLE and matched control subjects. Peak rIL2-induced proliferation was significantly decreased (mean reduction of 58%) in 5 of the 10 patients with SLE. Five of six patients with SLE studied for phytohemagglutinin-induced IL2 receptors had acquisition of IL2 receptors comparable to that of the control subjects. Some patients with SLE have a defect in rIL2-induced proliferation of their "resting" PBM that seems unrelated to a concomitant defect in phytohemagglutinin-induced IL2 receptor acquisition. This finding suggests that the defect in rIL2-induced proliferation may be due to either an abnormality in postreceptor signaling or an impairment in induction of high-affinity IL2 receptors.