Peripheral blood mononuclear cells of 10 out of 26 patients with human immunodeficiency virus type 1 (HIV-1) released IgE-binding factors, as determined by two independent assays. The formation of the factors by the mononudear cells was enhanced by incubation of the cells with homologous IgE. In the presence of IgE, peripheral blood mononuclear cells from 15 of the 26 patients formed a detectable amount of IgE-binding factors, whereas those of normal individuals or allergic rhinitis patients failed to do so. The major source of IgE-binding factors was the T cells of the HIV-1-infected patients. The CD8 + T cells from a HIV-1-infected patient formed IgE-binding factors upon incubation with IgE, and type II receptors for FcE were detected on both CD4' T cells and CD8' T cells in one of five patients studied.It was also found that culture supernatants of mononuclear cells from HIV-1-infected patients released soluble factors that induce normal human T cells to form IgE-binding factors. The results suggest that lymphocytes of some HIV-1-infected patients are activated to produce lymphokines regulating formation of IgE-binding factors.Previous experiments have shown that peripheral blood mononuclear cells (PBMCs) from ragweed-sensitive allergic individuals released soluble factors having affinity for IgE when the cells were incubated with allergen together with human IgE (1). Activation of normal PBMCs with phytohemagglutinin followed by incubation of the activated T cells with IgE also induced the formation of IgE-binding factors (IgE-BF). Young et al. (2) established FcE receptor-positive (FcR+) human T-cell clones from a patient with atopic dermatitis and found that these clones released IgE-BF.