The mast cell as a source of cytokines in asthma

The mast cell as a source of cytokines in asthma
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DOI:
10.1111/j.1749-6632.1996.tb32589.x
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发表时间:
1996-01-01
期刊:
CYTOKINES AND ADHESION MOLECULES IN LUNG INFLAMMATION
影响因子:
--
通讯作者:
Holgate, ST
Holgate, ST
中科院分区:
其他
文献类型:
--
作者:
Bradding, P;Holgate, ST

文献摘要

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肥大细胞参与许多不同的生物学和病理过程,包括组织重塑、伤口修复、纤维化、血管生成、凝血和宿主对肿瘤的反应。然而,肥大细胞与过敏性疾病的关系得到了最广泛的研究。众所周知,特定过敏原与肥大细胞结合的 IgE 交联会引发一系列事件,最终导致组胺等预先形成的介质以及新生成的自体物质 PGD 和 LTC4 的分泌。这些分子发挥许多与哮喘气道阻塞相关的作用,并且实际上它们作用的拮抗作用减弱了对过敏原激发的早期哮喘反应。然而,过敏原激发后的晚期反应(LPR)及其相关的炎症细胞流入被认为更类似于慢性哮喘,并且肥大细胞稳定药物(例如α-激动剂)尽管能够抑制自体激素释放,但未能抑制这种LPR,许多人认为这表明肥大细胞不能参与过敏性粘膜炎症的发展。在过去几年中,越来越明显的是,肥大细胞是许多多功能细胞因子的来源,这重新激发了人们对这种细胞作为协调器以及过敏性炎症事件的直接效应器的兴趣。
The mast cell has been implicated in many diverse biological and pathological processes including tissue remodeling, wound repair, fibrosis, angiogenesis, clotting, and host reactions to neoplasia. However, it is in relation to allergic disease that the mast cell has been most extensively studied. It is well established that cross-linking of mast-cell-bound IgE by specific allergen sets in motion a sequence of events culminating in the secretion of preformed mediators such as histamine, and the newly generated autacoids PGD, and LTC4. These molecules exert many effects relevant to the airway obstruction of asthma, and indeed antagonism of their effects attenuates the early asthmatic response to allergen provocation. However, it is the late-phase response (LPR) following allergen challenge with its associated inflammatory cell influx that is thought to more closely resemble chronic asthma, and the failure of mast-cellstabilizing drugs such as the &-agonists to inhibit this LPR in spite of their ability to inhibit autacoid release, was taken by many to indicate that mast cells could not be involved in the development of allergic mucosal inflammation. In the last few years it has become apparent that mast cells are the source of many multifunctional cytokines, which has revitalized interest in this cell as an orchestrator as well as an immediate effector of allergic inflammatory events.