每年出版 6 期
ISSN 打印: 1040-8401
ISSN 在线: 2162-6472
Indexed in
Mechanisms of IgE Elevation in HIV-1 Infection
摘要
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.
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