针对结合CD28的葡萄球菌肠毒素B作为抑制超抗原介导肠表皮屏障功能障碍的新策略
Carola Amormino1, Emanuela Russo1, Valentina Tedeschi1
1Department of Biology and Biotechnologies "Charles Darwin", Sapienza University of Rome, Rome, Italy.
Frontiers in immunology
|March 21, 2024
概括
黄金葡萄球菌肠毒素B (SEB) 触发T细胞,导致肠道炎症和屏障损伤. 一个新的 (pSEB116-132) 阻断了SEB.
科学领域:
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
- 胃肠病学 胃肠病学
背景情况:
- 黄金葡萄球菌分泌肠毒素,导致食物中毒和肠道损伤.
- 葡萄球菌肠毒素B (SEB) 作为超抗原,结合T细胞受体 (TCR) 和CD28,刺激炎症性细胞因子的释放.
- T细胞介导的SEB活动对肠上皮质完整性的影响尚未完全理解.
研究的目的:
- 研究T细胞衍生炎性细胞因子在SEB诱导的肠上皮功能障碍中的作用.
- 阐明SEB诱导的上皮质屏障破坏背后的分子机制.
- 确定针对SEB介导肠道炎症的治疗策略.
主要方法:
- 刺激SEB的T细胞,并评估分泌的炎症性细胞因子.
- 对Caco-2肠上皮细胞暴露于SEB激活的T细胞超级生物.
- 对表皮屏障完整性,actin细胞骨架,细胞-细胞结合以及表皮-介质细胞转换 (EMT) 转录因子 (EMT-TFs) 的分析.
- 核因子-κB (NF-κB) 和STAT3信号通路的研究.
- 基于结构的设计和测试SEB模仿性 (pSEB116-132) 针对CD28结合部位.
主要成果:
- 由SEB刺激的T细胞释放炎症性细胞因子,通过破坏actin细胞骨架和降低细胞-细胞结合的调节,损害Caco-2细胞屏障功能.
- 由SEB激活的T细胞通过NF-κB和STAT3信号传递诱导肠道上皮细胞中的EMT-TFs.
- 酸pSEB116-132有效地阻断了SEB与CD28的结合,减轻了SEB引起的上皮屏障功能障碍.
结论:
- 由SEB引发的T细胞介导的炎症显著导致肠上皮质屏障受损.
- 在肠道上皮细胞中,NF-κB和STAT3通路对于调解SEB诱导的EMT至关重要.
- 针对SEB-CD28与pSEB116-132等的相互作用,为SEB诱导的肠炎提供了潜在的治疗方法.
关键词:
CD28 CD28 CD28 CD28 CD28 CD28 CD28 CD28 CD28 CD28 CD28 CD28 CD28 CD28 CD28 CD28 CD28 CD28在T细胞,T细胞.这是一种炎症炎症炎症炎症.肠上皮质屏障功能障碍 肠上皮质屏障功能障碍葡萄球菌肠内毒素B (SEB) 的存在.超抗原 (s) 是指超抗原 (s) 的存在.更多相关视频
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