Mechanisms of IgE elevation in HIV-1 infection

Citation
G. Marone et al., Mechanisms of IgE elevation in HIV-1 infection, CR R IMMUN, 20(6), 2000, pp. 477-496
Citations number
139
Language
INGLESE
art.tipo
Review
Categorie Soggetti
Immunology
Journal title
CRITICAL REVIEWS IN IMMUNOLOGY
ISSN journal
1040-8401 → ACNP
Volume
20
Issue
6
Year of publication
2000
Pages
477 - 496
Database
ISI
SICI code
1040-8401(2000)20:6<477:MOIEIH>2.0.ZU;2-L
Abstract
Serum IgE levels are high in adults and children with HIV-1 infection and c ould be a marker of poor prognosis. Allergic reactions and adverse reaction s to drugs also tend to increase in HIV-1-infected individuals. An imbalanc e between a "T(H)1-like" and a "T(H)2-like" cytokine profile has been docum ented in HIV-1 infection. We have demonstrated that HIV-1 gp120 from differ ent clades is a stimulus for histamine and cytokine (IL-4 and IL-13) releas e 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+ ce lls. Human basophils and mast cells express the chemokine receptor CCR3, wh ich binds the chemokines eotaxin and RANTES. By interacting with the CCR3 r eceptor on Fc epsilon RI+ cells, HIV-1 Tat protein is a potent chemoattract ant for human basophils and lung mast cells. Preincubation of basophils wit h Tat protein upregulates mRNA CCR3 and the surface expression of this chem okine receptor. Tat also induces IL-4 and IL-13 release from basophils. Ext racellular 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. Our results indicate two novel mechanisms by which two HIV-1 proteins, gp120 and Tat, trigger the release of cytokines critical for T(H )2 polarization from human Fc epsilon RI+ cells.