期刊文献+

脓毒症中调控髓源性抑制细胞的非编码RNA及相关受体研究进展

Research progress on non‑coding RNA and related receptors regulating myeloid‑derived suppressor cells in sepsis
原文传递
导出
摘要 髓源性抑制细胞(MDSC)在脓毒症早期能够限制过度炎症反应,但在脓毒症晚期加剧免疫抑制。文章主要综述了MDSC在脓毒症发展过程中受微RNA(miRNA)‑21、miRNA‑181b、miRNA‑375、miRNA‑150、Hotairm1等非编码RNA(ncRNA)及白细胞介素‑1受体(IL‑1R)、Toll样受体(TLR)、肿瘤坏死因子受体(TNFR)、程序性细胞死亡受体‑1(PD‑1)、G蛋白耦联胆汁酸受体5(TGR5)、肝脏X受体(LXR)和CC趋化因子受体2(CCR2)等受体调控,从而发挥免疫抑制作用,为寻找治疗脓毒症的靶标提供一定的理论依据。 Myeloid‑derived suppressor cell(MDSC)are capable of limiting hyper‑inflammation during the early stages of sepsis,but exacerbate immunosuppression in the late stages of sepsis.This paper mainly reviews that,during the development of sepsis,MDSC are regulated by non‑coding RNAs such as microRNA(miRNA)‑21,miRNA‑181b,miRNA‑375,miRNA‑150 and Hotairm1,as well as receptors such as interleukin‑1 receptor(IL‑1R),Toll‑like receptor(TLR),tumor necrosis factor receptors(TNFR),programmed cell death receptor‑1(PD‑1),G protein‑coupled bile acid receptor(TGR5),liver X receptor(LXR),and C‑C motif chemokine receptor 2(CCR2),thereby exerting immune‑suppressing effect.These findings provide certain theoretical evidence for searching the therapeutic targets for sepsis.
作者 陆梦娇 张家祺 曹永兵 颜天华 李玲 Lu Mengjiao;Zhang Jiaqi;Cao Yongbing;Yan Tianhua;Li Ling(School of Basic Medicine and Clinical Pharmacy,China Pharmaceutical University,Nanjing 210009,China;Department of Pharmacy,Shanghai Municipal Hospital of Traditional Chinese Medicine,Shanghai University of Traditional Chinese Medicine,Shanghai 200071,China;Institute of Vascular Disease,Shanghai TCM‑Integrated Hospital,Shanghai University of Traditional Chinese Medicine,Shanghai 200082,China)
出处 《国际麻醉学与复苏杂志》 CAS 2024年第2期196-202,共7页 International Journal of Anesthesiology and Resuscitation
基金 上海市自然科学基金(21ZR1460400) 上海市中医药三年行动计划[ZY(2021-2023)-0203-04]。
关键词 髓源性抑制细胞 脓毒症 非编码RNA 受体 Myeloid‑derived suppressor cell Sepsis Non‑coding RNA Receptor
  • 相关文献

参考文献2

二级参考文献22

  • 1Medzhitov R, Preston-Hurlburt P, Janeway C, et al. A human homologue of the Drosophila Toll protein signals activation of adaptive immunity. Nature, 1997, 388(6640): 323-324.
  • 2Kim HM, Park BS, Kim JI, et al. Crystal structure of the TLR4- MD-2 complex with bound endotoxin antagonist Eritoran. Cell, 2007, 130(5): 906-917.
  • 3Akira S, Takeda K. Toll-like receptor signaling. Nat Rev Immunol, 2004, 4(7): 499-511.
  • 4Miggin SM, O'Neill LA. New insights into the regulation of signaling. J Leukoc Biol, 2006, 80(2): 220-226.
  • 5Poltorak A, He X, Smirnova I, et al. Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: mutations in TLR4 gene. Science, 1998, 282(5396): 2085-2088.
  • 6Hoshino K, Takeuchi O, Kawai T, et al. Cutting edge: Toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: evidence for TLR4 as the Lps gene product. J Immunol, 1999, 162(7): 3749-3752.
  • 7Smirnoval I, Hamblin MT, McBride C, et al. Excess of rare amino acid polymorphisms in the Toll-like receptor 4 in humans. Genetics, 2001, 158(4): 1657-1664.
  • 8Arbour NC, Lorenz E, Schutte BC, et al. TLR4 mutations are associated with endotoxin hyporesponsiveness in humans. Nat Genet, 2000, 25(2): 187-191.
  • 9Agnese DM, Calvano JE, Hahm SJ, et al. Human toll-like receptor 4 mutations but not CD14 polymorphisms are associated with an increased risk of gram-negative infections. J Infect Dis, 2002, 186 (10) : 1522-1525.
  • 10Lorenz E, Mira JP, Frees KL, et al. Relevance of mutations in the TLR4 receptor in patients with gram-negative septic shock. Arch Intern Med, 2002, 162(9): 1028-1032.

共引文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部