Role of human Fc epsilon RI+ cells in HIV-1 infection

Citation
G. Marone et al., Role of human Fc epsilon RI+ cells in HIV-1 infection, IMMUNOL REV, 179, 2001, pp. 128-138
Citations number
108
Language
INGLESE
art.tipo
Review
Categorie Soggetti
Immunology
Journal title
IMMUNOLOGICAL REVIEWS
ISSN journal
0105-2896 → ACNP
Volume
179
Year of publication
2001
Pages
128 - 138
Database
ISI
SICI code
0105-2896(200102)179:<128:ROHFER>2.0.ZU;2-C
Abstract
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 sw itch toward a "T(H)2-like" cytokine pattern. HIV-1 gp120 from different cla des is a potent stimulus for histamine release from human basophils and mas t cells. Gp 120 also induces IL-4 and IL-13 synthesis from basophils. It fu nctions as a viral superantigen by interacting with the V(H)3 region of IgE to induce mediator release from human Fc epsilon RI+ 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 Fc epsilon RI+ cells, HIV-1 Tar protein is a potent chemoattractant for bas ophils and lung mast cells. Tar protein also induces IL-4 and IL-13 release from basophils. Incubation of basophils with Tat protein upregulates the s urface expression of the CCR3 receptor, a co-receptor of HIV-1 infection. E xtracellular Tat affects the directional migration of human Fc epsilon RIcells, CCR3 expression and T(H)2 cytokines release. We have shown that HIV- 1 proteins gpl20 and Tat trigger the release of cytokines critical for T(H) 2 polarization from Fc epsilon RI+ cells through two distinct mechanisms. I n addition, Tat upregulates the beta -chemokine receptor CCR3, making Fc ep silon RI+ cells more susceptible to infection with CCR3 tropic HIV-1 isolat es.