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ISSN 打印: 1040-8401
ISSN 在线: 2162-6472

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DOI: 10.1615/CritRevImmunol.v20.i6.40
20 pages

Mechanisms of IgE Elevation in HIV-1 Infection

Gianni Marone
Division of Clinical Immunology and Allergy, University of Naples Federico II, Naples, Italy
Giovanni Florio
Division of Clinical Immunology and Allergy, University of Naples Federico II, Naples, Italy
Massimo Triggiani
Division of Clinical Immunology and Allergy, University of Naples Federico II, Naples, Italy
Angelica Petraroli
Division of Clinical Immunology and Allergy, University of Naples Federico II, Naples, Italy
Amato de Paulis
Division of Clinical Immunology and Allergy, University of Naples Federico II, Naples, Italy

ABSTRACT

Serum IgE levels are high in adults and children with HIV-1 infection and could be a marker of poor prognosis. Allergic reactions and adverse reactions to drugs also tend to increase in HIV-1-infected individuals. An imbalance between a "TH1-like" and a "TH2-like" cytokine profile has been documented in HIV-1 infection. We have demonstrated that HIV-1 gp120 from different clades is a stimulus for histamine and cytokine (IL-4 and IL-13) release from basophils. Gp120 acts as a viral superantigen, interacting with the VH3 region of IgE to induce mediator release from human FcεRI+ cells. Human basophils and mast cells express the chemokine receptor CCR3, which binds the chemokines eotaxin and RANTES. By interacting with the CCR3 receptor on FcεRI+ cells, HIV-1 Tat protein is a potent chemoattractant for human basophils and lung mast cells. Preincubation of basophils with Tat protein upregulates mRNA CCR3 and the surface expression of this chemokine receptor. Tat also induces IL-4 and IL-13 release from basophils. Extracellular Tat can influence the directional migration of human FcεRI+ cells, the expression of chemokine receptor CCR3, and the release of TH2 cytokines. Our results indicate two novel mechanisms by which two HIV-1 proteins, gp120 and Tat, trigger the release of cytokines critical for TH2 polarization from human FcεRI+ cells.