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首页> 外文期刊>Journal of Molecular Biology >How Inflammasomes Inform Adaptive Immunity
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How Inflammasomes Inform Adaptive Immunity

机译：炎症瘤如何通知适应性免疫力

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Abstract An immune response consists of a finely orchestrated interplay between initial recognition of potential microbial threats by the innate immune system and subsequent licensed adaptive immune neutralization. The initial recognition integrates environmental cues derived from pathogen-associated molecular patterns and cell-intrinsic damage-associated molecular patterns to contextualize the insult and inform a tailored adaptive response via T and B lymphocytes. While there are much data to support the role of transcriptional responses downstream of pattern recognition receptors in informing the adaptive immune response, markedly less attention has been paid to the role of post-translational responses to pathogen-associated molecular pattern and damage-associated molecular pattern recognition by the innate immune system, and how this may influence adaptive immunity. A well-characterized post-translational consequence of pattern recognition receptor signaling is the assembly of a multimeric signaling platform, termed the inflammasome, by members of the nucleotide-binding oligomerization domain (Nod), leucine-rich repeat-containing receptors (NLRs), and pyrin and HIN domain (PYHIN) families. Inflammasomes assemble in response to cytosolic perturbations, such as mitochondrial dysfunction and aberrant ion fluxes in the case of the canonical NLRP3 inflammasome or the presence of bacterial lipopolysaccharides in the case of the non-canonical inflammasome. Assembly of the inflammasome allows for the cleavage and activation of inflammatory caspases. These activated inflammatory caspases in turn cleave pro-form inflammatory cytokines into their mature bioactive species and lead to unconventional protein secretion and lytic cell death. In this review, we discuss evidence for inflammasome-mediated instruction and contextualization of infectious and sterile agents to the adaptive immune system. Graphical Abstract Display Omitted Highlights ? Interleukin-1 (IL-1) family cytokines play varying and essential roles in T cell-mediated responses during infection, vaccination, autoimmunity, and cancer. ? Inflammasomes are important regulators of IL-1 family cytokine activity and release. ? Most stimulators of inflammasome activity cause IL-1 release from pyroptotic cells, but recent studies identified inflammasomes that permit IL-1 release from living cells. ? Cells that release IL-1 while maintaining viability have been identified as “hyperactive” and are highly potent activators of adaptive immunity.
机译：摘要免疫反应包括在初始识别潜在的微生物威胁之间由先天免疫系统和随后的许可的适应性免疫中和之间的精确策划相互作用。初始识别将来自病原体相关的分子模式和细胞内在损伤相关的分子模式的环境提示整合，以使损害的侵蚀性，并通过T和B淋巴细胞通知定制的适应性反应。虽然存在许多数据来支持模式识别受体下游的转录反应的作用，但在通知适应性免疫应答时，已显着关注翻译后反应对病原体相关的分子模式和损伤相关分子模式的作用天生免疫系统的识别，以及如何影响自适应免疫力。特征在于模式识别受体信号传导的良好的翻译后果，是通过核苷酸结合寡聚化结构域（NOD），富含含亮氨酸的重复受体（NLRS）的成员称为炎症组的组装。和吡喃和欣域（Pyhin）家庭。炎症剂响应于细胞溶质扰动，例如在非典型炎症的情况下，在规范NLRP3炎性的情况下或在非规范炎症的情况下存在细菌脂多糖的情况。炎性组的组装允许切割和激活炎症性血糖。这些活化的炎症性血糖酶反转裂解炎症细胞因子进入其成熟的生物活性物质，并导致非传统的蛋白质分泌和裂解细胞死亡。在本次综述中，我们讨论炎症介导的指示和传染性和无菌剂的语境化对自适应免疫系统的证据。图形抽象显示省略了亮点？白细胞介素-1（IL-1）家族细胞因子在感染，疫苗接种，自身免疫和癌症期间在T细胞介导的反应中起不同和必要的作用。还是炎症是IL-1家族细胞因子活动和释放的重要调节因素。还是大多数炎症活动的刺激剂导致IL-1从糊化细胞中释放，但最近的研究确定了允许IL-1从活细胞中释放的炎症。还是释放IL-1同时保持活力的细胞已被鉴定为“过度活性”并且是适应性免疫的高效活化剂。

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