Regulation of human mast cell and basophil function by anaphylatoxins C3a and C5a.
Regulation of human mast cell and basophil function by anaphylatoxins C3a and C5a.
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DOI：
10.1016/j.imlet.2009.10.007
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发表时间：
2010-01-18
影响因子：
4.4
通讯作者：
Ali, Hydar
中科院分区：
文献类型：
--
作者：
Ali, Hydar
关键词：
过敏性疾病，如哮喘，是遗传易感个体对常见环境过敏原不适当的免疫反应造成的。在过敏原暴露后，树突状细胞（DC）与CD4+ T细胞的相互作用导致Th2细胞因子的产生，Th2细胞因子诱导B细胞合成IgE分子（致敏期）。这些IgE分子与肥大细胞和嗜碱性细胞表面的高亲和受体（FcεRI）结合，随后与过敏原交联，释放预先形成的和新合成的介质，引起支气管收缩、肺部炎症和哮喘（效应期）气道高反应性（AHR）。哮喘患者肺部补体成分C3a和C5a水平升高，可能是由过敏原和肥大细胞蛋白酶共同作用产生的。啮齿类动物的体内研究表明，虽然C3a在某些模型中促进过敏原致敏，但C5a抑制这种反应。尽管存在这种差异，但两种过敏毒素在体内均可促进肺部炎症和AHR，这表明除DC和T细胞外，其他细胞可能介导C3a和C5a在哮喘中的功能作用。本文综述了C3a和C5a在哮喘发病机制中的作用，特别强调肥大细胞和嗜碱性粒细胞。它讨论了过敏毒素激活肥大细胞和嗜碱性细胞的机制以及相关的信号通路，通过这些信号通路，它们的受体受到启动和脱敏的调节。
Allergic diseases such as asthma result from inappropriate immunologic responses to common environmental allergens in genetically susceptible individuals. Following allergen exposure, interaction of dendritic cells (DC) with CD4+ T cells leads to the production of Th2 cytokines, which induce B cells to synthesize IgE molecules (sensitization phase). These IgE molecules bind to their high affinity receptors (FcεRI) on the surface of mast cells and basophils and their subsequent cross-linking by allergen results in the release of preformed and newly synthesized mediators, which cause bronchoconstriction, lung inflammation and airway hyperresponsiveness (AHR) in asthma (effector phase). The complement components C3a and C5a levels are increased in the lungs of patients with asthma and are likely generated via the actions of both allergen and mast cell proteases. In vivo studies with rodents have shown that while C3a facilitates allergen sensitization in some models C5a inhibits this response. Despite this difference, both anaphylatoxins promote lung inflammation and AHR in vivo indicating that cells other than DC and T cells likely mediate the functional effects of C3a and C5a in asthma. This review focuses on the contribution of C3a and C5a in the pathogenesis of asthma with a particular emphasis on mast cells and basophils. It discusses the mechanisms by which anaphylatoxins activate mast cells and basophils and the associated signaling pathways via which their receptors are regulated by priming and desensitization.
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影响因子：
4.4
作者：
Ali, H;Ahamed, J;Patel, DD
通讯作者：
Patel, DD
影响因子：
4.4
作者：
Baelder, R;Fuchs, B;Braun, A
通讯作者：
Braun, A
DOI：
10.1073/pnas.87.17.6813
发表时间：
1990-09-01
影响因子：
11.1
作者：
BISCHOFF, SC;DEWECK, AL;DAHINDEN, CA
通讯作者：
DAHINDEN, CA
影响因子：
3.4
作者：
Blease, Kate;Lewis, Alan;Raymon, Heather K
通讯作者：
Raymon, Heather K
影响因子：
5.8
作者：
Ali H;Panettieri RA Jr
通讯作者：
Panettieri RA Jr