Role of mast cells and basophils in chronic rhinosinusitis.

Role of mast cells and basophils in chronic rhinosinusitis.
复制标题

DOI:
10.3109/9781420014020-10
复制
发表时间:
2007
期刊:
Clinical allergy and immunology
影响因子:
--
通讯作者:
R. Pawankar;Kun‐Hee Lee;M. Nonaka;R. Takizawa
R. Pawankar;Kun‐Hee Lee;M. Nonaka;R. Takizawa
中科院分区:
其他
文献类型:
--
作者:
R. Pawankar;Kun‐Hee Lee;M. Nonaka;R. Takizawa

文献摘要

相似文献

肥大细胞和嗜碱性细胞通过多种机制参与诱导和/或维持嗜酸性粒细胞炎症,包括ige依赖性和ige非依赖性过程。后者包括最近才被阐明的各种刺激,包括由细菌、病毒、真菌、补体或自身抗体触发的机制。MCs和嗜碱性细胞通过直接释放炎症介质、细胞因子和生长因子以及间接激活结构细胞来促进炎症。越来越多的证据表明,MCs(很可能还有嗜碱性粒细胞)在CRS的发病机制中,特别是在NP的发病和进展中,处于重要地位(图1)。非过敏性CRS/NP中嗜酸性粒细胞炎症的潜在机制是有趣的,而不是传统的ige依赖性MCs激活。虽然目前的药理学方法不可能完全分离MCs或嗜碱性粒细胞在CRS和NP发病机制中的作用,但这些方法最终很可能是可行的。可以预期,这些细胞中的一个或两个将发挥重要作用,特别是考虑到它们被IgE和非IgE机制激活的潜力,它们产生广泛的炎症介质,细胞因子和生长因子,以及它们独特的蛋白酶组合。
Mast cells and basophils contribute to induction and/or maintenance of eosinophilic inflammation by a variety of mechanisms, including IgE-dependent and IgE-independent processes. The latter include a variety of stimuli that have only recently been elucidated, including mechanisms triggered by bacteria, virus, fungi, complement, or autoantibodies. MCs, and basophils contribute to inflammation both directly through the release of inflammatory mediators, cytokines and growth factors and indirectly through the activation of structural cells. Accumulating evidence places MCs (and most probably basophils) in a position of importance in the pathogenesis of CRS, particularly in the pathogenesis and progression of NP (Fig. 1). Mechanisms other than conventional IgE-dependent activation of MCs are intriguing as potential mechanisms of eosinophilic inflammation in non-allergic CRS/NP. Although it is not possible using current pharmacologic approaches to completely isolate the effects of MCs or basophils in CRS and NP pathogenesis, it seems most likely that such approaches will eventually be available. It might be expected that one or both of these cells will be shown to play important roles, particularly considering their potential for activation by IgE and non-IgE mechanisms, their production of a broad array of inflammatory mediators, cytokines and growth factors, and their unique assortment of proteases.