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炎症和微生物转移与艾滋病毒感染者的MAIT细胞减少有关

Angela Ryu¹, Brian M Clagett¹, Michael L Freeman^1,2

¹Rustbelt Center for AIDS Research, Division of Infectious Diseases and HIV Medicine, Department of Medicine, Case Western Reserve University/University Hospitals Cleveland Medical Center, Cleveland, OH.

Pathogens & immunity

|December 5, 2024

概括

艾滋病毒感染者接受抗逆转录病毒疗法而免疫不响应的人具有较少的粘膜关联不变T细胞 (MAIT). 炎症和微生物转移通过降低IL-7响应能力损害MAIT细胞功能,使这些情况恶化.

科学领域:

免疫学免疫学免疫学
微生物学微生物学
传染性疾病传染性疾病

背景情况:

粘膜关联不变T细胞 (MAIT) 对于控制微生物感染至关重要.
接受抗逆转录病毒疗法 (ART) 的艾滋病毒感染者 (PWH) 可以被分为免疫反应者 (IR) 或免疫不响应者 (INR).
与IR相比,INR表现出较低的MAIT细胞数量,升高的全身炎症和增加的微生物转移.

研究的目的:

研究MAIT细胞数量,炎症和ART上的PWH中的微生物转位之间的关系.
阐明炎症和微生物转移影响MAIT细胞的机制.

主要方法:

在IR,INR和HIV阴性对照中使用流细胞计数来计算和特征MAIT细胞.
斯皮尔曼分析评估了MAIT细胞数量与血中的炎症标志物/微生物遗传序列之间的相关性.
在体外测定和分析用托西利祖马布 (TCZ) 治疗的PWH被用于探索IL-6和IL-7信号通路.

主要成果:

MAIT细胞数与炎症标志物 (IL-6,IP-10) 和微生物转位标志物 (CD14,LPS,FABP2) 有负相关性.
血中特定细菌遗传序列 (Serratia,Proteobacteria) 的丰富程度与较低的MAIT细胞数相关.
用TCZ阻断IL-6信号传递增加了MAIT细胞上的IL-7受体表达,并减少了血IL-7,表明IL-7吸收得到改善.

结论:

在ART上PWH中的炎症和微生物转移有助于MAIT细胞耗尽.
在MAIT细胞中IL-7响应能力受损是关键机制,它将炎症,微生物转位和MAIT细胞损失联系在一起.
这就形成了一个恶性循环,即增加了INR中的微生物转移和炎症.

关键词:

艾滋病病毒艾滋病病毒艾滋病病毒在IL-6的研究中,IL-6被认为是IL-6的基因.炎症炎症是一种炎症.一个 MAIT 细胞.微生物转位的转位是微生物转位.托西利兹马巴姆 (Tocilizumab) 是一种

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