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天然免疫细胞可以识别外源病原体刺激,产生炎性细胞因子,TNF-α是其中重要的一种。大量的炎性细胞因子会促发过激的免疫反应并导致组织损伤,因此,炎性细胞因子调控机制的研究一直是免疫学研究的一个重点。内毒素耐受是机体抑制过量炎性细胞因子产生的一种重要保护机制。细胞或机体给予内毒素预处理可以抑制随后的内毒素刺激产生的炎性细胞因子,从而保护细胞或机体免于内毒素的毒性作用,此现象即为内毒素耐受。关于内毒素耐受的分子机制,目前认为机体可通过产生负向调控蛋白,如SOCS1、IRAK-M和SHIP-1等,抑制TLR信号,导致内毒素耐受。此外,一些miRNA(如miR9、miR155等)也可抑制TLR信号及其下游炎性细胞因子的产生;而染色质水平的修饰,如组蛋白修饰和核
Natural immune cells can recognize foreign pathogens to stimulate, produce inflammatory cytokines, TNF-α is one of the important. A large number of inflammatory cytokines can trigger an exacerbated immune response and lead to tissue damage. Therefore, the research on the regulatory mechanism of inflammatory cytokines has been a focus of immunological research. Endotoxin tolerance is an important protective mechanism that the body inhibits the production of excessive inflammatory cytokines. Endotoxin preconditioning by cells or by the body inhibits the production of inflammatory cytokines by subsequent endotoxin stimulation and thereby protects the cells or body from the toxic effects of endotoxins, which are endotoxin tolerant. Concerning the molecular mechanism of endotoxin tolerance, it is currently believed that the body can inhibit TLR signaling by producing negative regulatory proteins such as SOCS1, IRAK-M and SHIP-1, leading to endotoxin tolerance. In addition, some miRNAs (such as miR9, miR155, etc.) also inhibit TLR signaling and downstream inflammatory cytokines; and chromatin level modifications, such as histone modification and nuclear