4.6 Article

Mucosal-Associated Invariant T (MAIT) Cells Are Highly Activated and Functionally Impaired in COVID-19 Patients

期刊

VIRUSES-BASEL
卷 13, 期 2, 页码 -

出版社

MDPI
DOI: 10.3390/v13020241

关键词

COVID-19; SARS-CoV-2; mucosal-associated invariant T (MAIT) cells

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资金

  1. Deutsche Forschungsgemeinschaft (DFG) [424774790]
  2. Else Kroner-Fresenius-Stiftung
  3. Bavarian State Ministry for Science and the Arts

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MAIT cells in patients with COVID-19 show high activation and expression of proinflammatory cytokines, while their antibacterial and antiviral function is impaired. The data points towards the importance of MAIT cells in the pathogenesis of COVID-19.
Coronavirus disease 2019 (COVID-19), caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), comprises mild courses of disease as well as progression to severe disease, characterised by lung and other organ failure. The immune system is considered to play a crucial role for the pathogenesis of COVID-19, although especially the contribution of innate-like T cells remains poorly understood. Here, we analysed the phenotype and function of mucosal-associated invariant T (MAIT) cells, innate-like T cells with potent antimicrobial effector function, in patients with mild and severe COVID-19 by multicolour flow cytometry. Our data indicate that MAIT cells are highly activated in patients with COVID-19, irrespective of the course of disease, and express high levels of proinflammatory cytokines such as IL-17A and TNF alpha ex vivo. Of note, expression of the activation marker HLA-DR positively correlated with SAPS II score, a measure of disease severity. Upon MAIT cell-specific in vitro stimulation, MAIT cells however failed to upregulate expression of the cytokines IL-17A and TNF alpha, as well as cytolytic proteins, that is, granzyme B and perforin. Thus, our data point towards an altered cytokine expression profile alongside an impaired antibacterial and antiviral function of MAIT cells in COVID-19 and thereby contribute to the understanding of COVID-19 immunopathogenesis.

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