Mitochondria, the dynamic organelles and power house of eukaryotic cells function as metabolic hubs of cells undergoing continuous cycles of fusion and fission. Recent findings have made it increasingly apparent that mitochondria essentially involved in energy production have evolved as principal intracellular signaling platforms regulating not only innate immunity but also inflammatory responses. Perturbations in mitochondrial dynamics, including fusion/fission, electron transport chain (ETC) architecture and cristae organization have now been actively correlated to modulate metabolic activity and immune function of innate and adaptive immune cells. Several newly identified mitochondrial proteins in mitochondrial outer membrane such as mitochondrial antiviral signaling protein (MAVS) and with mitochondrial DNA acting as danger-associated molecular pattern (DAMP) and mitochondrial ROS generated from mitochondrial sources have potentially established mitochondria as key signaling platforms in antiviral immunity in vertebrates and thereby orchestrating adaptive immune cell activations respectively. A thorough understanding of emerging and intervening role of mitochondria in toll-like receptor-mediated innate immune responses and NLRP3 inflammasome complex activation has gained lucidity in recent years that advocates the imposing functions of mitochondria in innate immunity. Fascinatingly, also how the signals stemming from the endoplasmic reticulum co-operate with the mitochondria to activate the NLRP3 inflammasome is now looked ahead as a stage to unravel as to how different mitochondrial and associated organelle stress responses co-operate to bring about inflammatory consequences. This has also opened avenues of research for revealing mitochondrial targets that could be exploited for development of novel therapeutics to treat various infectious, inflammatory, and autoimmune disorders. Thus, this review explores our current understanding of intricate interplay between mitochondria and other cellular processes like autophagy in controlling mitochondrial homeostasis and regulation of innate immunity and inflammatory responses.

中文翻译：

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线粒体：先天免疫力不可缺少的参与者和炎症反应的守护者。

线粒体是真核细胞的动态细胞器和动力室，是经历连续融合和裂变循环的细胞的代谢枢纽。最近的发现使得越来越明显的是，基本上参与能量产生的线粒体已经进化为主要的细胞内信号传递平台，不仅调节先天免疫，而且调节炎症反应。线粒体动力学的扰动，包括融合/裂变，电子传输链（ETC）结构和cr组织，现已被积极地关联起来，以调节先天和适应性免疫细胞的代谢活性和免疫功能。线粒体外膜中的几种新近鉴定的线粒体蛋白（例如线粒体抗病毒信号蛋白（MAVS））以及线粒体DNA充当危险相关分子模式（DAMP）和由线粒体来源产生的线粒体ROS已潜在地确立了线粒体作为抗病毒免疫的关键信号传递平台在脊椎动物中，从而分别协调适应性免疫细胞活化。近年来，对线粒体在收费样受体介导的先天性免疫应答和NLRP3炎性小体复合物激活中的新兴作用和介入作用的透彻了解，使人们更加清楚了线粒体在先天性免疫中的作用。令人着迷的是 内质网产生的信号如何与线粒体协同激活NLRP3炎性体，现在也被展望为一个阶段，以探讨线粒体和相关细胞器应激反应如何协同作用引起炎症后果。这也为揭示线粒体靶标开辟了研究途径，可以将线粒体靶标用于开发用于治疗各种传染性，炎性和自身免疫性疾病的新型疗法。因此，本综述探讨了我们目前对线粒体与其他细胞过程（例如自噬）在控制线粒体体内稳态以及调节先天免疫和炎症反应之间复杂相互作用的理解。