Marone G, Florio G, Petraroli A, Triggiani M, de Paulis A
Division of Clinical Immunology and Allergy, University of Naples Federico II, Italy.
Immunol Rev. 2001 Feb;179:128-38. doi: 10.1034/j.1600-065x.2001.790113.x.
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 "TH2-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 VH3 region of IgE to induce mediator release from human FcepsilonRI+ 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 FcepsilonRI+ 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 FcepsilonRI+ cells, CCR3 expression and TH2 cytokines release. We have shown that HIV-1 proteins gp120 and Tat trigger the release of cytokines critical for TH2 polarization from FcepsilonRI+ cells through two distinct mechanisms. In addition, Tat upregulates the beta-chemokine receptor CCR3, making FcepsilonRI+ cells more susceptible to infection with CCR3 tropic HIV-1 isolates.
成人和儿童感染HIV-1后血清IgE水平升高可能是预后不良的一个标志。据信，HIV-1感染涉及向“类TH2”细胞因子模式的转变。来自不同分支的HIV-1 gp120是人类嗜碱性粒细胞和肥大细胞释放组胺的有效刺激物。Gp120还可诱导嗜碱性粒细胞合成IL-4和IL-13。它通过与IgE的VH3区域相互作用，作为病毒超抗原发挥作用，从而诱导人FcepsilonRI+细胞释放介质。趋化因子受体CCR3可结合趋化因子嗜酸性粒细胞趋化蛋白和RANTES，由嗜碱性粒细胞和肺肥大细胞表达。通过与FcepsilonRI+细胞上的CCR3受体相互作用，HIV-1 Tat蛋白是嗜碱性粒细胞和肺肥大细胞的有效趋化剂。Tat蛋白还可诱导嗜碱性粒细胞释放IL-4和IL-13。用Tat蛋白孵育嗜碱性粒细胞可上调CCR3受体的表面表达，CCR3受体是HIV-1感染的共受体。细胞外Tat影响人FcepsilonRI+细胞的定向迁移、CCR3表达和TH2细胞因子释放。我们已经表明，HIV-1蛋白gp120和Tat通过两种不同机制触发FcepsilonRI+细胞释放对TH2极化至关重要的细胞因子。此外，Tat上调β趋化因子受体CCR3，使FcepsilonRI+细胞更容易感染CCR3嗜性HIV-1分离株。
