HTNV infection induces activation and deficiency of CD8+MAIT cells in HFRS patients.
HTNV infection induces activation and deficiency of CD8+MAIT cells in HFRS patients.
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HTNV 感染诱导 HFRS 患者 CD8 MAIT 细胞活化和缺陷
DOI：
10.1093/cei/uxac111
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发表时间：
2023-03-08
影响因子：
4.6
通讯作者：
中科院分区：
文献类型：
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作者：
汉滩病毒（HTNV）感染引起肾综合征出血热（HFRS）的流行，主要发生在亚洲。粘膜相关不变T（MAIT）细胞是一种先天性T淋巴细胞，在病毒感染过程中发挥重要作用。然而，它们在HTNV感染过程中的作用和表型尚未被探索。我们基于scRNA-seq数据结合流式细胞术数据表征了来自HFRS患者的CD 8 +MAIT细胞。我们发现HTNV感染引起外周血中CD 8 +MAIT细胞的丢失和活化，这与疾病的严重程度相关。CD 8 +MAIT细胞能产生颗粒酶B和IFN-γ，并能抑制HTNV在内皮细胞中的复制，表明CD 8 +MAIT细胞具有抗HTNV的活性。此外，HTNV或HTNV暴露的单核细胞对MAIT细胞的体外感染表明MAIT细胞的活化是IL-18介导的。总之，本研究首次确定了MAIT细胞的基因表达谱，提供了HTNV感染期间MAIT细胞激活的潜在分子机制，并提出了MAIT细胞在HFRS中的潜在抗病毒作用。HTNV感染引起外周血中MAIT细胞的活化和缺乏。从MAIT细胞产生IFN-γ可以限制HTNV的复制。MAIT细胞的活化由IL-18介导，IL-18来源于HTNV感染的单核细胞。
Hantaan virus (HTNV) infection causes an epidemic of hemorrhagic fever with renal syndrome (HFRS) mainly in Asia. Mucosal-associated invariant T (MAIT) cells are innate-like T lymphocytes known to play an important role in innate host defense during virus infection. However, their roles and phenotypes during HTNV infection have not yet been explored. We characterized CD8+MAIT cells from HFRS patients based on scRNA-seq data combined with flow cytometry data. We showed that HTNV infection caused the loss and activation of CD8+MAIT cells in the peripheral blood, which were correlated with disease severity. The production of granzyme B and IFN-γ from CD8+MAIT cells and the limitation of HTNV replication in endothelia cells indicated the anti-viral property of CD8+MAIT cells. In addition, in vitro infection of MAIT cells by HTNV or HTNV-exposed monocytes showed that the activation of MAIT cells was IL-18 mediated. In conclusion, this study identified, for the first time, gene expression profiles of MAIT cells, provided underlying molecular mechanisms for activation of MAIT cells during HTNV infection, and suggested a potential anti-viral role of MAIT cells in HFRS. HTNV infection caused the activation and deficiency of MAIT cells in the peripheral blood. The production of IFN-γ from MAIT cells can limit the replication of HTNV. The activation of MAIT cells was mediated by IL-18, which was sourced from monocytes infected by HTNV.
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