Role of human FcεRI+ cells in HIV-1 infection.

Enhanced serum IgE levels in adults and children with HIV-1 infection could be a marker of poor prognosis. HIV-1 infection is believed to involve a switch toward a "T[subH]2-like" cytokine pattern. HIV-1 gp120 from different clades is a potent stimulus for histamine release from human basophils and mast cells. Gp120 also induces IL-4 and IL-13 synthesis from basophils. It functions as a viral superantigen by interacting with the V[subH]3 region IgE to induce mediator release from human FcεRI[sup+] cells. The chemokine receptor CCR3, which binds the chemokines eotaxin and RANTES, is expressed by basophils and lung mast cells. By interacting with the CCR3 receptor on FcεRI[sup+] cells, HIV-1 Tat protein is a potent chemoattractant for basophils and lung mast cells. Tat protein also induces IL-4 and IL-13 release from basophils. Incubation of basophils with Tat protein upregulates the surface expression of the CCR3 receptor, a co-receptor of HIV-1 infection. Extracellular Tat affects the directional migration of human Fc&epsilonRI[sup+] cells, CCR3 expression and T[subH]2 cytokines release. We have shown that HIV-1 proteins gp120 and Tat trigger the release of cytokines critical for T[subH]2 polarization from FcεRI[sup+] cells through two distinct mechanisms. In addition, Tat upregulates the β-chemokine receptor CCR3, making FcεRI[sup+] cells more susceptible to infection with CCR3 tropic HIV-1 isolates. [ABSTRACT FROM AUTHOR]