Mast cells (MCs) have historically been considered masters of allergy, but there is substantial evidence supporting their contribution to tissue microorganism clearance. Their activation through the cross-linking of bound IgE provokes mast cell degranulation and activates tyrosine kinase (Syk and Lyn), leading to cytokine/chemokine generation and release. Current consensus holds that mast cells participate in the body's defense against numerous pathogens, including bacteria, fungi, viruses and parasites, but also contribute to the inflammatory response induced by these biological agents. In the light of the latest findings, we describe the cross-talk between mast cells and pathogenic microorganisms. This review summarizes our current understanding of the host immune response, with emphasis on the roles of MCs and the cytokine/chemokine network in provoking inflammation and generating protective immunity. This review addresses the ability of microorganisms to activate MCs provoking inflammation. We describe some MC-specific biological activities related to infections and discuss the evidence of MC mechanisms involved in the microbial activation which cause cytokine/chemokine generation-mediated inflammation, and provide a description of novel functions of mast cells during microbial infection. Interleukin (IL)-37 binds the α chain of the IL-18 receptor and suppresses MyD88-mediated inflammatory responses. IL-37 plays a pathological role in certain infections by inhibiting the production of pro-inflammatory cytokines, such as IL-1 and TNF. Here we report the interrelationship between IL-37, inflammatory cytokines and mast cells. Our report offers opportunities for the design of new therapeutic interventions in inflamed tissue induced by microorganism infections, acting on manipulation of mast cells and/or inflammatory cytokine blockage.

中文翻译：

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肥大细胞对入侵微生物的病理生理学，炎症和防御机制的最新进展：IL-37的抑制作用。

肥大细胞（MCs）历来被认为是过敏的主人，但是有大量证据支持它们对组织微生物清除的贡献。它们通过结合的IgE的交联而激活，引起肥大细胞脱粒并激活酪氨酸激酶（Syk和Lyn），从而导致细胞因子/趋化因子的产生和释放。目前的共识认为，肥大细胞参与机体对多种病原体的防御，包括细菌，真菌，病毒和寄生虫，但也有助于这些生物因子引起的炎症反应。根据最新发现，我们描述了肥大细胞与致病微生物之间的串扰。这篇综述总结了我们目前对宿主免疫反应的了解，着重于MC和细胞因子/趋化因子网络在引发炎症和产生保护性免疫方面的作用。这项审查解决了微生物激活引起炎症的MC的能力。我们描述了与感染有关的某些MC特异性生物学活性，并讨论了涉及微生物活化的MC机制的证据，这些机制引起细胞因子/趋化因子的产生介导的炎症，并提供了微生物感染过程中肥大细胞的新功能的描述。白介素（IL）-37结合IL-18受体的α链并抑制MyD88介导的炎症反应。IL-37通过抑制促炎性细胞因子（例如IL-1和TNF）的产生，在某些感染中起病理作用。在这里我们报告IL-37之间的相互关系，炎性细胞因子和肥大细胞。我们的报告为设计由微生物感染引起的发炎组织中的新治疗干预措施提供了机会，这些干预措施可用于肥大细胞的操纵和/或炎性细胞因子的阻滞。