Regulation of T cell proliferation by cloned interferon-α mediated by leu-11b-positive cells

The autologous T lymphocyte proliferative response (AMLR) induced by a B lymphocyte-enriched non-T, nonadherent cell population (NT, NAC) and by a macrophage-enriched population were both suppressed by the addition of a cloned interferon-α (IFN-αCon₁) directly to the cultures. Preincubation of the stimulating NT, NAC with IFN-αCon₁ resulted in comparable suppression. In contrast, preincubation of the macrophages with IFN-αCon₁ resulted in significant augmentation of T cell proliferation. Depletion of Leu-11b-positive cells from the NT, NAC exposed to IFN-αCon₁ restored the autologous T cell response. Addition of IFN-αCon₁ activated Leu-11b-positive cells, isolated from the NT, NAC population, was suppressive of the AMLR. Although NK cytotoxicity was irradiation sensitive, suppression of the AMLR by IFN-αCon₁-activated NT, NAC was resistant, suggesting that different subsets of cells or mechanisms by the same cells may have been responsible. These observations may offer insights into the potential role of cells with the NK phenotype, Leu-11b, and IFN in contributing to immunoregulatory changes observed in clinical states associated with elevated concentrations of IFN.