IL-1β是一种重要的炎性细胞因子，树突状细胞（DC）是其重要来源。细胞外微环境酸化是一种引起细胞应激的常见危险信号。申报者前期研究已证实，酸敏感离子通道（ASIC）是DC感知酸化刺激的受体，并介导酸化诱导的DC成熟。申报者预试验结果显示，酸化可促进DC分泌IL-1β，该效应可被ASIC通道阻断剂amiloride阻断，但其机制不明。申报者据此推测，酸化介导的ASIC活化可诱导炎症小体形成，从而在促进DC分泌IL-1β中发挥重要作用。本项目拟探讨ASIC激活炎症小体的作用，阐明酸化介导DC分泌活性IL-1β的分子机制。本项目可望进一步阐明病理状态中微环境酸化调控DC功能的作用及其机制，并为探讨某些免疫相关疾病发生发展的机制提供新的实验依据。

Interleukin 1β (IL-1β) is an important proinflammatory cytokine.The primary sources are dendritic cells.Extracellular acidosis is a common danger signal that play a role as cell stress. We have found that Acid-Sensing Ion Channels expressed by DC could be activated by low pH and contributed to the maturation of DCs induced by acidosis.Also, we found that IL-1β could be secreted by DCs induced by acidosis, and the secretion could be abolished by ASICs blocker amiloride,but the mechanism is not clear.We hypothesize that activated inflammasomes induced by ASICs result in IL-1β secretion of DCs.We plan to investigate the mechanisms of ASICs-inflammasomes signal pathway in IL-1β secretion of DCs stimulated by acidosis.The results could expand our knowledge on DCs functions under inflammatory circumstance.