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  • 1
    Electronic Resource
    Electronic Resource
    Copenhagen : Munksgaard International Publishers
    Immunological reviews 179 (2001), S. 0 
    ISSN: 1600-065X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary: 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 “TH2-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 VH3 region of IgE to induce mediator release from human FcεRI+ 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+ 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 FcεRI+ cells, CCR3 expression and TH2 cytokines release. We have shown that HIV-1 proteins gp120 and Tat trigger the release of cytokines critical for TH2 polarization from FcεRI+ cells through two distinct mechanisms. In addition, Tat upregulates the β-chemokine receptor CCR3, making FcεRI+ cells more susceptible to infection with CCR3 tropic HIV-1 isolates.This paper is dedicated to Rita Levi-Montalcini who first suggested an involvement of FcεRI+ cells in HIV-1 infection. This work was supported by a grant from the Istituto Superiore Sanità (AIDS project 40B.64 and 40A.67), CNR (Target project Biotechnology No. 99.00216.PF31 and No. 99.00401. PF49) and MURST (Rome, Italy).
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 524 (1988), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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