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Role of human FcεRI + cells in HIV‐1 infection
Author(s) -
Marone Gianni,
Florio Giovanni,
Petraroli Angelica,
Triggiani Massimo,
De Paulis Amato
Publication year - 2001
Publication title -
immunological reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.839
H-Index - 223
eISSN - 1600-065X
pISSN - 0105-2896
DOI - 10.1034/j.1600-065x.2001.790113.x
Subject(s) - ccr3 , biology , chemokine , chemokine receptor , receptor , cytokine , immunoglobulin e , immunology , microbiology and biotechnology , immune system , antibody , biochemistry
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 “T H 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 H 3 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 T H 2 cytokines release. We have shown that HIV‐1 proteins gp120 and Tat trigger the release of cytokines critical for T H 2 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).