Innate cells and T helper 2 cell immunity in airway inflammation.

Innate cells and T helper 2 cell immunity in airway inflammation.
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DOI:
10.1016/j.immuni.2009.08.014
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发表时间:
2009-09-18
期刊:
影响因子:
32.4
通讯作者:
Austen, K. Frank
Austen, K. Frank
中科院分区:
医学1区
文献类型:
--
作者:
Barrett, Nora A.;Austen, K. Frank

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活化的肥大细胞、嗜酸性粒细胞和嗜碱性粒细胞浸润哮喘患者的气道,这是过度兴奋的辅助性T细胞2(Th2)免疫应答的结果,其驱动IgE的产生,引发肥大细胞和嗜碱性粒细胞,并促进组织嗜酸性粒细胞增多和肥大细胞增生。最近的证据表明,这些先天性效应物可以在这种经典的Th2细胞范例之外被激活,并且它们在促进先天性和适应性肺部炎症的发展中具有额外的作用。气道上皮细胞在协调变应性肺部炎症中的作用也受到重视。来自基础研究的新数据强调了许多独特的途径参与气道粘膜表面复杂的天然过敏原和微生物引发的炎症。在这里,我们审查的作用,效应细胞和气道上皮细胞在增强,有时,绕过传统的Th2细胞介导的过敏性炎症。
Activated mast cells, eosinophils, and basophils infiltrate the airways of asthmatics as a result of an overexuberant T helper 2 (Th2) cell immune response that drives the production of IgE, primes mast cells and basophils, and promotes tissue eosinophilia and mast cell hyperplasia. Recent evidence demonstrates that these innate effectors can be activated outside of this classical Th2 cell paradigm and that they have additional roles in promoting the development of innate and adaptive pulmonary inflammation. There is also an appreciation for the role of airway epithelial cells in orchestrating allergic pulmonary inflammation. Emerging data from basic research highlights the involvement of many unique pathways in the inflammation triggered by complex native allergens and microbes at the airway mucosal surface. Here we review the role of effector cells and airway epithelial cells in augmenting and, at times, bypassing traditional Th2 cell-mediated allergic inflammation.
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