艾滋病毒-1感染对神素-1-酸盐受体产生影响 1 人类胆小板的调节失调
Rachel S Resop1,2, Bradley Salvatore1, Shawn J Kim1
1Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA 90095, USA.
International journal of molecular sciences
|September 28, 2023
概括
艾滋病毒-1感染对人胸腺中的S1P受体1 (S1PR1) 进行上调,可能导致T细胞过早退出. 这会影响艾滋病毒感染者 (PLWH) 接受ART的免疫功能.
科学领域:
- 免疫学 免疫学 免疫学
- 病毒学 病毒学
- 细胞生物学 细胞生物学
背景情况:
- 功能性T淋巴细胞的再生对于艾滋病毒感染者 (PLWH) 来说至关重要,即使在抗逆转录病毒疗法 (ART) 上.
- 关于HIV-1对胸腺前体进入和T淋巴细胞从胸腺退出的影响的数据有限.
- 斯芬哥辛-1-酸盐 (S1P) 信号调节了原始乳腺细胞的退出.
研究的目的:
- 为了研究HIV-1对S1P信号传递和T细胞从胸腺外出的影响.
- 为了确定HIV-1感染是否会影响人类胸腺中S1P受体1 (S1PR1) 的表达.
主要方法:
- 在实验室中使用初级人体胸细胞的研究.
- 在人性化小鼠模型的体内和体外研究.
- 在受感染的胸膜组织中分析S1PR1表达和细胞因子概况.
主要成果:
- 艾滋病毒-1 感染在人胸腺中调节S1PR1的表达,无论是内心感染还是全身感染.
- 细胞因子调节失调,特别是干扰素-β (IFN-β) 和瘤坏死因子-α (TNF-α),与增加的S1PR1表达相关.
- 感染了人性化小鼠的脏中成熟和不成熟的T细胞增加的存在表明了提摩细胞的加速退出.
结论:
- 艾滋病毒-1 感染通过提升胸腺中S1PR1的调节来破坏S1P信号的调节.
- 这种上调可能会导致胸细胞的加速或增加退出,包括不成熟的T细胞.
- 功能性不成熟的T细胞的过早退出可能会损害PLWH的免疫功能.
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