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合成人TLR9-LRR11肽通过与CpG寡脱氧核苷酸结合并因此减少其内化来减弱TLR9信号传导。

Synthetic Human TLR9-LRR11 Peptide Attenuates TLR9 Signaling by Binding to and thus Decreasing Internalization of CpG Oligodeoxynucleotides.

作者信息

Pan Xichun, Li Bin, Kuang Mei, Liu Xin, Cen Yanyan, Qin Rongxin, Ding Guofu, Zheng Jiang, Zhou Hong

机构信息

Department of Pharmacology, College of Pharmacy, the Third Military Medical University, Chongqing 400038, China.

Medical Research Center, Southwestern Hospital, the Third Military Medical University, Chongqing 400038, China.

出版信息

Int J Mol Sci. 2016 Feb 22;17(2):242. doi: 10.3390/ijms17020242.

Abstract

Toll-like receptor (TLR) 9 is an endosomal receptor recognizing bacterial DNA/CpG-containing oligodeoxynucleotides (CpG ODN). Blocking CpG ODN/TLR9 activity represents a strategy for therapeutic prevention of immune system overactivation. Herein, we report that a synthetic peptide (SP) representing the leucine-rich repeat 11 subdomain of the human TLR9 extracellular domain could attenuate CpG ODN/TLR9 activity in RAW264.7 cells by binding to CpG ODN and decreasing its internalization. Our results demonstrate that preincubation with SP specifically inhibited CpG ODN- but not lipopolysaccharide (LPS)- and lipopeptide (PAM3CSK4)-stimulated TNF-α and IL-6 release. Preincubation of SP with CpG ODN dose-dependently decreased TLR9-driven phosphorylation of IκBα and ERK and activation of NF-κB/p65. Moreover, SP dose-dependently decreased FAM-labeled CpG ODN internalization, whereas non-labeled CpG ODN reversed the inhibition. The KD value of SP-CpG ODN binding was within the micromolar range. Our results demonstrated that SP was a specific inhibitor of CpG ODN/TLR9 activity via binding to CpG ODN, leading to reduced ODN internalization and decreased activation of subsequent pathways within cells. Thus, SP could be used as a potential CpG ODN antagonist to block TLR9 signaling.

摘要

Toll样受体9(TLR9)是一种识别含细菌DNA/含CpG的寡脱氧核苷酸(CpG ODN)的内体受体。阻断CpG ODN/TLR9活性是一种治疗性预防免疫系统过度激活的策略。在此,我们报告一种代表人类TLR9细胞外结构域富含亮氨酸重复序列11亚结构域的合成肽(SP),可通过与CpG ODN结合并减少其内化来减弱RAW264.7细胞中的CpG ODN/TLR9活性。我们的结果表明,用SP预孵育可特异性抑制CpG ODN刺激的肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)释放,但不抑制脂多糖(LPS)和脂肽(PAM3CSK4)刺激的释放。SP与CpG ODN预孵育可剂量依赖性地降低TLR9驱动的IκBα和细胞外信号调节激酶(ERK)磷酸化以及核因子-κB(NF-κB)/p65的激活。此外,SP剂量依赖性地降低了荧光素标记的CpG ODN内化,而非标记的CpG ODN可逆转这种抑制作用。SP-CpG ODN结合的解离常数(KD)值在微摩尔范围内。我们的结果表明,SP是一种通过与CpG ODN结合来特异性抑制CpG ODN/TLR9活性的抑制剂,导致ODN内化减少以及细胞内后续信号通路激活降低。因此,SP可作为一种潜在的CpG ODN拮抗剂来阻断TLR9信号传导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3104/4783973/c750568aa89e/ijms-17-00242-g001.jpg

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