Mast cells (MCs) are critically involved in microbial defense by releasing antimicrobial peptides (such as cathelicidin LL-37 and defensins) and phagocytosis of microbes. In past years, it has become evident that in addition MCs may eliminate invading pathogens by ejection of web-like structures of DNA strands embedded with proteins known together as extracellular traps (ETs). Upon stimulation of resting MCs with various microorganisms, their products (including superantigens and toxins), or synthetic chemicals, MCs become activated and enter into a multistage process that includes disintegration of the nuclear membrane, release of chromatin into the cytoplasm, adhesion of cytoplasmic granules on the emerging DNA web, and ejection of the complex into the extracellular space. This so-called ETosis is often associated with cell death of the producing MC, and the type of stimulus potentially determines the ratio of surviving vs. killed MCs. Comparison of different microorganisms with specific elimination characteristics such as S pyogenes (eliminated by MCs only through extracellular mechanisms), S aureus (removed by phagocytosis), fungi, and parasites has revealed important aspects of MC extracellular trap (MCET) biology. Molecular studies identified that the formation of MCET depends on NADPH oxidase-generated reactive oxygen species (ROS). In this review, we summarize the present state-of-the-art on the biological relevance of MCETosis, and its underlying molecular and cellular mechanisms. We also provide an overview over the techniques used to study the structure and function of MCETs, including electron microscopy and fluorescence microscopy using specific monoclonal antibodies (mAbs) to detect MCET-associated proteins such as tryptase and histones, and cell-impermeant DNA dyes for labeling of extracellular DNA. Comparing the type and biofunction of further MCET decorating proteins with ETs produced by other immune cells may help provide a better insight into MCET biology in the pathogenesis of autoimmune and inflammatory disorders as well as microbial defense.

肥大细胞（MCs）通过释放抗菌肽（如cathelicidin LL-37和防御素）和吞噬微生物而关键参与微生物防御。在过去的几年中，很明显，此外，MCs 可以通过喷射嵌入被称为细胞外陷阱 (ETs) 的蛋白质的 DNA 链的网状结构来消除入侵的病原体。在用各种微生物、它们的产物（包括超抗原和毒素）或合成化学物质刺激静止的 MCs 后，MCs 被激活并进入一个多阶段过程，包括核膜解体、染色质释放到细胞质中、细胞质颗粒粘附在新兴的 DNA 网上，并将复合物喷射到细胞外空间。这种所谓的 ETosis 通常与产生 MC 的细胞死亡有关，刺激的类型可能决定存活与死亡 MC 的比率。比较具有特定消除特性的不同微生物，例如化脓性链球菌（仅通过细胞外机制被 MCs 消除）、金黄色葡萄球菌（通过吞噬作用去除）、真菌和寄生虫揭示了 MC 细胞外陷阱 (MCET) 生物学的重要方面。分子研究发现，MCET 的形成取决于 NADPH 氧化酶产生的活性氧 (ROS)。在这篇综述中，我们总结了目前关于 MCETosis 的生物学相关性及其潜在的分子和细胞机制的最新技术。我们还概述了用于研究 MCET 的结构和功能的技术，包括使用特定单克隆抗体 (mAb) 检测 MCET 相关蛋白（如类胰蛋白酶和组蛋白）的电子显微镜和荧光显微镜，以及细胞不可渗透的 DNA 染料细胞外DNA的标记。