The neutrophil-activating protein of Helicobacter pylori (HP-NAP) as an immune modulating agent
The neutrophil-activating protein of Helicobacter pylori (HP-NAP) as an immune modulating agent
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DOI：
10.1111/j.1574-695x.2007.00258.x
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发表时间：
2007-07-01
影响因子：
--
通讯作者：
de Bernard, Marina
中科院分区：
文献类型：
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作者：
D'Elios, Mario Milco;Amedei, Amedeo;de Bernard, Marina
在进化过程中，微生物已经发展了几种免疫调节策略。幽门螺杆菌嗜中性粒细胞激活蛋白（HP-NAP）是一种毒力因子，吸引并激活中性粒细胞，促进其内皮粘附和氧自由基和趋化因子（包括CXCL 8、CCL 3和CCL 4）的产生。HP-NAP是一种TLR 2激动剂，是一种能够诱导人中性粒细胞和单核细胞表达白细胞介素-12（IL-12）和IL-23的免疫调节剂。事实上，HP-NAP具有将抗原特异性T细胞应答从占优势的Th 2转变为极化的Th 1细胞毒性表型的潜力，其特征在于高水平的干扰素-γ和肿瘤坏死因子-α产生。因此，HP-NAP是驱动H.幽门螺杆菌感染，并可能是一个新的工具，为未来的治疗策略，旨在重新定向Th 2到Th 1的反应，例如在特应性，疫苗和癌症免疫治疗。
During evolution microorganisms have developed several immune modulating strategies. The Helicobacter pylori neutrophil-activating protein (HP-NAP) is a virulence factor that attracts and activates neutrophils, and promotes their endothelial adhesion and the production of oxygen radicals and chemokines, including CXCL8, CCL3 and CCL4. HP-NAP, a TLR2 agonist, is an immune modulator able to induce the expression of interleukin-12 (IL-12) and IL-23 by human neutrophils and monocytes. In fact, HP-NAP has the potential to shift antigen-specific T-cell responses from a predominant Th2 to a polarized Th1 cytotoxic phenotype, characterized by high levels of interferon-gamma and tumor necrosis factor-alpha production. Thus, HP-NAP is a key factor driving Th1 inflammation in H. pylori infection and may be a new tool for future therapeutic strategies aimed at redirecting Th2 into Th1 responses, for example in atopy, vaccinology and cancer immunotherapy.