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10.3390/cells9081750

http://scihub22266oqcxt.onion/10.3390/cells9081750
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32707842!7464076!32707842
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suck abstract from ncbi


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pmid32707842      Cells 2020 ; 9 (8): ä
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  • Defining the CD39/CD73 Axis in SARS-CoV-2 Infection: The CD73(-) Phenotype Identifies Polyfunctional Cytotoxic Lymphocytes #MMPMID32707842
  • Ahmadi P; Hartjen P; Kohsar M; Kummer S; Schmiedel S; Bockmann JH; Fathi A; Huber S; Haag F; Schulze Zur Wiesch J
  • Cells 2020[Jul]; 9 (8): ä PMID32707842show ga
  • The ectonucleotidases CD39 and CD73 regulate immune responses by balancing extracellular ATP and adenosine in inflammation and are likely to be involved in the pathophysiology of COVID-19. Here, we analyzed CD39 and CD73 on different lymphocyte populations in a small cohort of COVID-19 patients and in healthy individuals. We describe a significantly lower level of expression of CD73 on cytotoxic lymphocyte populations, including CD8(+) T, natural killer T (NKT), and natural killer (NK) cells, during COVID-19. Interestingly, the decrease of CD73 on CD8(+) T cells and NKT cells correlated with serum ferritin levels. Furthermore, we observed distinct functional differences between the CD73(+) and CD73(-) subsets of CD8(+) T cells and NKT cells with regard to cytokine/toxin secretion. In COVID-19 patients, the majority of the CD73(-)CD8(+) T cells were capable of secreting granzyme B, perforin, tumor necrosis factor (TNF-alpha) or interferon-gamma (IFN-gamma). To conclude, in this first study of CD39 and CD73 expression of lymphocytes in COVID-19, we show that CD8(+) T cells and NKT cells lacking CD73 possess a significantly higher cytotoxic effector functionality compared to their CD73(+) counterparts. Future studies should investigate differences of cellular CD39 and CD73 expression in patients at different disease stages and their potential as prognostic markers or targets for immunomodulatory therapies.
  • |5'-Nucleotidase/*metabolism[MESH]
  • |Adenosine/metabolism[MESH]
  • |Adult[MESH]
  • |Aged[MESH]
  • |Apyrase/*metabolism[MESH]
  • |Betacoronavirus[MESH]
  • |COVID-19[MESH]
  • |Coronavirus Infections/enzymology/*immunology[MESH]
  • |Female[MESH]
  • |GPI-Linked Proteins/metabolism[MESH]
  • |Granzymes/metabolism[MESH]
  • |Humans[MESH]
  • |Inflammation/enzymology/immunology[MESH]
  • |Interferon-gamma/metabolism[MESH]
  • |Killer Cells, Natural/*immunology[MESH]
  • |Male[MESH]
  • |Middle Aged[MESH]
  • |Natural Killer T-Cells/*immunology[MESH]
  • |Pandemics[MESH]
  • |Perforin/metabolism[MESH]
  • |Pneumonia, Viral/enzymology/*immunology[MESH]
  • |SARS-CoV-2[MESH]
  • |Signal Transduction/immunology[MESH]
  • |T-Lymphocytes, Cytotoxic/*immunology/metabolism[MESH]


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