The neutrophil-activating protein of Helicobacter pylori promotes Th1 immune responses
The neutrophil-activating protein of Helicobacter pylori promotes Th1 immune responses
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DOI：
10.1172/jci27177
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发表时间：
2006-04-01
影响因子：
15.9
通讯作者：
de Bernard, M
中科院分区：
文献类型：
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作者：
Amedei, A;Cappon, A;de Bernard, M
幽门螺杆菌嗜酸性激活蛋白（HP-NAP）是幽门螺杆菌的毒力因子。幽门螺旋杆菌，刺激中性粒细胞产生大量氧自由基并粘附于内皮细胞。我们在这里报告，HP-NAP是一种TLR 2激动剂，能够诱导中性粒细胞和单核细胞表达IL-12和IL-23。在抗原诱导的T细胞系中加入HP-NAP作为免疫调节剂，导致产生IFN-γ的T细胞数量显著增加，IL-4分泌细胞减少，从而使抗原活化的人T细胞的细胞因子谱从Th 2细胞毒性表型转变为Th 1细胞毒性表型。我们还发现，在体内HP-NAP引发了抗原特异性的Th 1极化的T细胞反应，在H.幽门螺杆菌感染患者这些数据表明HP-NAP是H. pylori能够引发先天免疫系统的细胞产生IL-12和IL-23，并且他们建议将其作为促进Th 1免疫应答的新工具。
The Helicobacter pylori neutrophil-activating protein (HP-NAP) is a virulence factor of H. pylori that stimulates in neutrophils high production of oxygen radicals and adhesion to endothelial cells. We report here that HP-NAP is a TLR2 agonist able to induce the expression of IL-12 and IL-23 by neutrophils and monocytes. Addition in culture of HP-NAP, as an immune modulator, to antigen-induced T cell lines resulted in a remarkable increase in the number of IFN-gamma-producing T cells and decrease of IL-4-secreting cells, thus shifting the cytokine profile of antigen-activated human T cells from Th2 to a Th1 cytotoxic phenotype. We also found that in vivo HP-NAP elicited an antigen-specific Th1-polarized T cell response in the gastric mucosa of H. pylori-infected patients. These data indicate HP-NAP as an important factor of H. pylori able to elicit cells of the innate immune system to produce IL-12 and IL-23, and they suggest it as a new tool for promoting Th1 immune responses.