Thymocytes that express the complete CD3−T-cell receptor (TCR) complex are CD4− and CD8−. The CD4+ T-cell population can be subdivided into at least two quite distinct subsets, TH1 and TH2 cells, based upon cytokine expression. Interleukin-1 (IL-1) appears to be required for optimal proliferation of T cells in response to antigen and it seems that in the absence of IL-1, TH2 clones proliferate less in response to antigen. Tenidap is an antirheumatic agent that has an inhibitory effect on IL-1 production. In these studies, we show that isolated human peripheral blood mononuclear cells (PBMCs) treated in vitro with Tenidap (15 μg/mL) for 48-h incubations significantly (p < 0.05) enhanced the present of CD4+ expression compared with untreated cells (control), as determined by cytofluorimetric analysis. Lipopolysaccharide and Bacillus Calmette-Guérin were used as positive controls. When the cells were tested for CD3 or CD8 receptor expression, no differences were found between the untreated PBMCs and the treated (15 μg/mL Tenidap) cells. No change was found when cells were incubated for 72 h. Moreover, our data show a strong dose-dependent inhibitory effect of Tenidap (15 μg/mL) on IL-1α, IL-1β, and leukotriene B4 secretion in PBMCs treated overnight. The increased CD4+ expression by Tenidap in PBMCs may suggest an important role for this new antirheumatic agent in immunity and may hold future therapeutic promise for diseases involving IL-1 and leukotriene B4 as mediators.Key words: Tenidap, lymphocyte receptors, leukotriene B4, interleukin-1, lipopolysaccharide.
Release of interleukin-1 by peripheral blood mononuclear cells in patients with tuberculosis and active inflammation.
