Formation of IgE-binding factors by T cells of patients infected with human immunodeficiency virus type 1.

Abstract

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.

Decreased serum levels of IgE and IgE-binding factors in individuals infected with HTLV-I

“…T cells from HTV-Iinfected patients were reported to release IgE BFs into their cultures (Carini et al, 1988). In the present study, however, the occurrence of FceRII on mononuclear cells from HTLV-Iinfected individuals was within normal range, and surprisingly, serum levels of IgE BFs were reduced in patients with ATL.…”

“…However, HTLV-Itransformed T cell line ED, which constitutively forms IgE BFs, responds to neither IL-4 nor IFN-y with enhanced biosynthesis of IgE BFs (Kawabe et al, 1988). Carini et al, (1988) reported that the culture supernatants of mononuclear cells from HIV-1-infected patients released another soluble factor that induced the formation of IgE BFs by normal human T cells. It is possible, therefore, that soluble factor(s) formed by mononuclear cells from HTLV-I-infected individuals may be involved in the formation of IgE BFs.…”

“…Subsequently, T cells in blood from patients with HIV-1 were found to release IgE BFs in vitro and mononuclear cells from HIV-1-infected patients also released soluble factor(s) involved in the production of IgE BFs (Carini et al, 1988). The idea of the similar tropism of the retroviruses, HIV-1 and HTLV-I, together with that mRNA encoding Fe«RII was detected in an HTLV-I-transformed T cell line (Kawabe et al, 1988), prompted us to examine the possibility that HTLV-I-infected individuals might be affected by altered IgE immunomechanism.…”

Binding site for IgE of the human lymphocyte low-affinity Fc epsilon receptor (Fc epsilon RII/CD23) is confined to the domain homologous with animal lectins.

“…It is found complexed with IgE in the serum of atopic patients (7) and its level is highly elevated in patients with B-cell-derived chronic lymphocytic leukemia (19). Furthermore, T cells of patients infected with human immunodeficiency virus type 1 are induced to produce IgE-BF (20).…”

Interleukin 7 and sCD23 Synergize in the Induction of Human T Cell Activation in HIV-1-Infected Subjects

“…Increased sCD23 in serum and synovial fluid in rheu matoid arthritis patients has been demonstrated [29], rais ing the question of the direct role o f sC'D23 in other dis eases. It has been previously reported that sCD23 is in creased in HI V-l infection [31][32][33][34], The fact that sCD23 has been reported to costimulate IFN-y production raises the possibility that sCD23 may play a pivotal role in the control of the immune response. Moreover, the receptors for IL-7 and CD23 have been found to be present lymphoid cells of HI V-l-infected subjects and on mitogen-stimulated T cells [25,26,[31][32][33][34].…”