Finally, blocking IL-33 receptors at the spinal level mediates analgesia during acute and chronic inflammatory pain, underscoring an important function of IL-33 in pain signaling. Collectively, our data reveal a critical role of the TLR2-IL-33 axis in innate immune activation for pain initiation and maintenance.doi:10....
The response of neutrophils to bacterial and fungal infections can be accelerated by an adaptive immune response to these pathogens. The IL-1-producing CD4+T helper cell subset Th17 cells is well described as a potent inducer of neutrophils12as such, Th17 cells are critical for immunity againstC...
另外,运 些受体通过与作为内源性的组织损伤因子的损伤相关分子模式(DAMPS)结合而被活化,从 而向细胞内传递信号。TLR2及化R4的活化例如经由作为转录因子的核因子kB(NF-kB)的活 化而诱导肿瘤坏死因子曰(TNFa)或白细胞介素6(IL-6)等炎症性的细胞活素的表达,从而引 起炎症应答(Nat. Immunol.、2010、V〇1.11、N...
利用 ELISA 实验技术检测了两种细胞在 LTA 刺激后肿瘤转移相关因子 VEGF、IL-6 和 TGF-β1 的表达情况以及在 TLR2 中和抗体封闭作用后两种细胞肿瘤转移相关因子的 表达分泌的变化情况,发现 LTA 刺激后 MDA-MB-231 细胞的 VEGF、IL-6 和 TGF-β1 I 山东师范大学硕士学位论文分泌量均明显提高,其提高幅度分别...
HEK-Blue-Lucia™ hTLR2 (NF/IL8) Cells (NF-κB-SEAP/KI-[IL-8]Lucia) NF-κB and IL-8 reporter HEK293 cells expressing human TLR2 Catalog code: hkd-htlr2ni https://www.invivogen.com/hek-blue-lucia-htlr2 For research use only Version 23E24-MM PRODUCT INFORMATION Content • ...
PorB formulation was necessary to induce a TNFα and IL-6 cytokine response (data not shown). Our group showed previously that PorB induces inreased MHC I and CD86 expression in BMDCs13. This might be a very important underlying molecular mechanism of PorB enhancing antigen specific T cell ...
磷酸化的 NF-κB参与的细胞功能,主要集中在抑制细胞凋亡和促进炎症因子(IL-6/IL-8/TNFa等)、炎症相关蛋白的表达。NF-κB作为一种信号分子,在机体生物效应过程中起调节作用,在机体免疫应答、炎症反应过程中针对细胞选择性扩增、选择性减少时发挥着主要效应。国外学者Beg AA等[7]研究发现NF-κB有抑制凋亡的功能。
研究显示,大肠埃希菌益生菌株Nissle 1917可通过TLR2和TLR4依赖的途径改善葡聚糖硫酸钠(DSS)诱导的小鼠结肠炎,丁酸梭菌则可以通过激活TLR2调节的骨髓分化因子88(MyD88)的非依赖性途径,引起NF-κB、IL-8、IL-6及TNF-α的分泌,以抵抗病原菌的感染同时防止自身免疫紊乱[37-38]。给断奶仔猪分别灌胃益生菌不拉氏酵...
These lysates underwent Western blot analysis to assess the protein expression levels of key pro-inflammatory cytokines [IL-6 (A) and TNF-α (B)], enzymes [COX-2 (C) and iNOS (D)], signaling pathways [p-p38 MAPK (E), p-NF-κB p65 (F), and p-STAT3 (G)], and NLRP4 ...
(IL)-6 by BMMs mediated through TLR2 activation was inhibited by RANKL and that the addition of sialidase restored TLR2 activity and the TNF-α and IL-6 levels; however, lipopolysaccharide (LPS) stimulation was not affected by RANKL or sialidase (Fig.S4). To examine the transcriptional ...