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Rosette inhibitory factor (RIF) augments cyclic AMP generation by helper T lymphocytes
The effect of Rosette Inhibitory Factor (RIF) on cyclic AMP generation by peripheral blood mononuclear cells (PBMC) and lymphocyte subpopulations (OKT4+ or helper T cells, OKT8+ or suppressor T cells, B lymphocytes) was analyzed. The results were compared to those observed with isoproterenol, an agent which is known to inhibit erythrocyte rosette (ER) formation and increase cyclic AMP levels in T cells. RIF elevated cyclic AMP levels in PBMC, an effect which was observed to be confined to helper T cells. Isoproterenol also elevated levels of cyclic AMP in PBMC but non-selectively augmented levels of the cyclic nucleotide in all lymphocyte subpopulations. Whereas isoproterenol increased cyclic AMP levels within 30 min, RIF did so after a lag period of 4 hr, a delay which is necessary for inhibition of ER formation. These studies reaffirm the selective effect of RIF on helper T cells. We conclude that inhibition of ER formation and possibly other immunoregulatory effects associated with RIF may be mediated via modulation of the adenyl cyclase-cyclic nucleotide network.
The effect of Rosette Inhibitory Factor (RIF) on cyclic AMP generation by peripheral blood mononuclear cells (PBMC) and lymphocyte subpopulations (OKT4+ or helper T cells, OKT8+ or suppressor T cells, B lymphocytes) was analyzed. The results were compared to those observed with isoproterenol, an agent which is known to inhibit erythrocyte rosette (ER) formation and increase cyclic AMP levels in T cells. RIF elevated cyclic AMP levels in PBMC, an effect which was observed to be confined to helper T cells. Isoproterenol also elevated levels of cyclic AMP in PBMC but non-selectively augmented levels of the cyclic nucleotide in all lymphocyte subpopulations. Whereas isoproterenol increased cyclic AMP levels within 30 min, RIF did so after a lag period of 4 hr, a delay which is necessary for inhibition of ER formation. These studies reaffirm the selective effect of RIF on helper T cells. We conclude that inhibition of ER formation and possibly other immunoregulatory effects associated with RIF may be mediated via modulation of the adenyl cyclase-cyclic nucleotide network.