炎性小体:修复牙周发病机制

Nazreen Ansari, J. Paul, J. D’lima, S. Parackal
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摘要

医学界最近被炎症小体的发现所困扰,炎症小体被认为是调节宿主免疫炎症反应的。它们被认为在这个过程中有许多目的,其中许多仍有待阐明。已经观察到,为了响应微生物成分PAMPs(病原体相关分子模式)或内源性分子DAMPs(损伤相关分子模式),需要某些传感器蛋白来组装这些炎症小体。在大多数情况下,炎性小体已经被证明要经历一个由两个步骤组成的过程才能被激活。此外,根据研究,这涉及到各种传感器蛋白家族,它们通过一些相应的途径在许多疾病的发病机制中发挥作用,包括牙周病。因此,这条信息为我们提供了进一步探索和寻找调节宿主对微生物挑战反应的新靶点的机会。
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The Inflammasomes: Revamping Periodontal Pathogenesis
The world of medicine has recently been flummoxed by the discovery of inflammasomes which are assumed to regulate the host immuno-inflammatory responses. They are believed to have a multitude of purposes in the process, many of which, still remain to be elucidated. It has been observed that certain sensor proteins are required to assemble these inflammasomes in response to microbial components called PAMPs (pathogen associated molecular patterns) or endogenous molecules called DAMPs (damage associated molecular patterns). In most cases, inflammasomes have been demonstrated to undergo a process consisting of two steps to get activated. Furthermore, according to research, this involves various families of sensor proteins which play a part in the pathogenesis of many diseases, including periodontal disease through a number of corresponding pathways. This piece of information, thereby, affords us the opportunity to explore further and search for new targets to modulate host responses to microbial challenges.
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