A defect of immunoregulatory T cell subsets in systemic lupus erythematosus patients demonstrated with anti-2H4 antibody

The cell surface phenotype of peripheral blood lymphocytes (PBL) of systemic lupus erythematosus (SLE) patients was characterized with the anti-2H4 monoclonal antibody that defines the human suppressor inducer subset. The T4⁺2H4⁺ population of cells has been shown to be critical for the activation of T8⁺ suppressor cells. Patients with SLE had a markedly decreased percentage of T4⁺2H4⁺ cells (13 ± 2%) in their PBL compared with normal controls (21 ± 1%) (P < 0.001). This reduction was greatest in patients with active SLE, especially those with renal disease. Serial analysis of patients with SLE and renal disease showed a correlation between percent positive circulating T4⁺2H4⁺ cells and disease activity. Moreover, there was a significant correlation between a low percentage of T4⁺2H4⁺ cells and decreased suppressor-inducer function in autologous mixed lymphocyte reaction-activated T4⁺ cells from SLE patients. Thus, a deficiency exists in SLE patients with active renal disease in the T4⁺2H4⁺ suppressor-inducer T cell subset.