Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Japan.
Cell Immunol. 2010;261(2):122-7. doi: 10.1016/j.cellimm.2009.11.009. Epub 2009 Dec 3.
The effect of a series of toll-like receptor (TLR) ligands on the production of nitric oxide (NO) in mouse B1 cells was examined by using CD5(+) IgM(+) WEHI 231 cells. The stimulation with a series of TLR ligands, which were Pam3Csk4 for TLR1/2, poly I:C for TLR3, lipopolysaccharide (LPS) for TLR4, imiquimod for TLR7 and CpG DNA for TLR9, resulted in enhanced NO production via augmented expression of an inducible type of NO synthase (iNOS). LPS was most potent for the enhancement of NO production, followed by poly I:C and Pam3Csk4. Imiquimod and CpG DNA led to slight NO production. The LPS-induced NO production was dependent on MyD88-dependent pathway consisting of nuclear factor (NF)-kappaB and a series of mitogen-activated protein kinases (MAPKs). Further, it was also dependent on the MyD88-independent pathway consisting of toll-IL-1R domain-containing adaptor-inducing IFN-beta (TRIF) and interferon regulatory factor (IRF)-3. Physiologic peritoneal B1 cells also produced NO via the iNOS expression in response to LPS. The immunological significance of TLR ligands-induced NO production in B1 cells is discussed.
用 CD5(+)IgM(+)WEHI 231 细胞检测了一系列 Toll 样受体 (TLR) 配体对小鼠 B1 细胞一氧化氮 (NO) 产生的影响。一系列 TLR 配体（Pam3Csk4 用于 TLR1/2、多聚 I:C 用于 TLR3、脂多糖 (LPS) 用于 TLR4、咪喹莫特用于 TLR7 和 CpG DNA 用于 TLR9）的刺激导致诱导型一氧化氮合酶 (iNOS) 的表达增强，从而导致 NO 产生增加。LPS 对 NO 产生的增强作用最有效，其次是多聚 I:C 和 Pam3Csk4。咪喹莫特和 CpG DNA 导致少量的 NO 产生。LPS 诱导的 NO 产生依赖于 MyD88 依赖性途径，该途径由核因子 (NF)-kappaB 和一系列丝裂原活化蛋白激酶 (MAPKs) 组成。此外，它还依赖于由 toll-IL-1R 结构域包含衔接子诱导 IFN-beta (TRIF) 和干扰素调节因子 (IRF)-3 组成的 MyD88 非依赖性途径。生理腹膜 B1 细胞也通过 LPS 诱导的 iNOS 表达产生 NO。讨论了 TLR 配体诱导的 B1 细胞中 NO 产生的免疫学意义。
