Defective T-lymphocyte colony formation in patients with lupus nephritis.

To determine whether patients with systemic lupus erythematosus (SLE) and active nephritis have more profound defects in cell-mediated immunity (CMI), we studied T-colony-forming cells (TCFC) in 12 patients with lupus nephritis (LN) and 14 patients with chronic mesangial proliferative glomerulonephritis (CGN) without renal insufficiency. We also examined the activity of T-colony-stimulating factor (TCSF) in media conditioned by phytohaemagglutinin (PHA) stimulated peripheral blood lymphocytes (PHA-LCM). The levels of TCFC and TCSF were decreased in patients with LN compared with those in normal controls and lower in LN patients with the nephrotic syndrome (NS) than in those without NS. In contrast, these CMI parameters in CGN patients with or without NS did not differ from normal subjects. TCSF activity for TCFC in both normal individuals and LN patients was removed from PHA-LCM with interleukin 2 (IL 2) receptor bearing cultured T cells. These in vitro findings suggest that IL 2 is the essential factor contained in PHA-LCM. Our observations may lend further insight into the understanding of the immunoregulatory defect in LN.