Dysregulation of the IgE/Fc epsilon RI network in HIV-1 infection

Citation
G. Marone et al., Dysregulation of the IgE/Fc epsilon RI network in HIV-1 infection, J ALLERG CL, 107(1), 2001, pp. 22-30
Citations number
58
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Immunology
Journal title
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
ISSN journal
0091-6749 → ACNP
Volume
107
Issue
1
Year of publication
2001
Pages
22 - 30
Database
ISI
SICI code
0091-6749(200101)107:1<22:DOTIER>2.0.ZU;2-U
Abstract
Serum IgE levels are increased in adults and children with HIV-1 infection and could be a marker of poor prognosis. Allergic reactions and adverse rea ctions to drugs are also increased in HIV-1-infected individuals.,in imbala nce between a T(H)1-like and a T(H)2-like cytokine profile has been documen ted in HIV-1 infection. we have found that HIV-1 gp120 from different clade s is a potent stimulus for histamine and cytokine (IL-4 and IL-13) release from basophils. Gp120 acts as a viral superantigen, interacting with the V( H)3 region of IgE to induce mediator release from human Fc epsilon RI+ cell s. Human basophils and mast cells express the chemokine receptor CCR3, whic h binds the chemokines eotaxin and RANTES. By interacting with the CCR3 rec eptor on Fc epsilon RI+ cells, HIV-1 Tat protein is a potent chemoattractan t for human basophils and lung mast cells. Tat protein also induced IL-4 an d IL-13 release from basophils, Preincubation of basophils with Tat protein upregulated the surface expression of the CCR3 receptor. Extracellular Tat can influence the directional migration of human Fc epsilon RI+ cells, the expression of chemokine receptor CCR3, and the release of T(H)2 cytokines, Because Tat protein is actively released by HIV-l-infected cells, our resu lts indicate a novel mechanism by which Fc epsilon RI+ cells are rendered m ore susceptible to infection with CCR3-tropic HIV-1 isolates; that is, two HIV-1 proteins, gp120 and Tat, trigger the release of cytokines critical fo r T(H)2 polarization from Fc epsilon RI+ cells, and Tat upregulates beta -c hemokine receptor CCR3 on these cells.