Functional exhaustion of antiviral lymphocytes in COVID-19 patients

Functional exhaustion of antiviral lymphocytes in COVID-19 patients

19 March 2020 | Meijuan Zheng, Yong Gao, Gang Wang, Guobin Song, Siyu Liu, Dandan Sun, Yuanhong Xu and Zhigang Tian
The study by Zheng et al. (2020) investigates the functional exhaustion of cytotoxic lymphocytes, such as cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells, in patients with COVID-19. The authors found that the total number of NK and CD8+ T cells was significantly reduced in patients with SARS-CoV-2 infection, and these cells exhibited functional exhaustion characterized by increased expression of NKG2A. In patients who recovered after therapy, the number of NK and CD8+ T cells increased, along with reduced NKG2A expression. These findings suggest that SARS-CoV-2 infection may lead to early breakdown of antiviral immunity through the functional exhaustion of cytotoxic lymphocytes. The study also highlights the potential role of NKG2A as a novel inhibitory molecule in immune checkpoint blockade, which could be targeted to prevent functional exhaustion and enhance virus elimination in the early stages of SARS-CoV-2 infection.The study by Zheng et al. (2020) investigates the functional exhaustion of cytotoxic lymphocytes, such as cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells, in patients with COVID-19. The authors found that the total number of NK and CD8+ T cells was significantly reduced in patients with SARS-CoV-2 infection, and these cells exhibited functional exhaustion characterized by increased expression of NKG2A. In patients who recovered after therapy, the number of NK and CD8+ T cells increased, along with reduced NKG2A expression. These findings suggest that SARS-CoV-2 infection may lead to early breakdown of antiviral immunity through the functional exhaustion of cytotoxic lymphocytes. The study also highlights the potential role of NKG2A as a novel inhibitory molecule in immune checkpoint blockade, which could be targeted to prevent functional exhaustion and enhance virus elimination in the early stages of SARS-CoV-2 infection.
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