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10.3389/fimmu.2021.602130

http://scihub22266oqcxt.onion/10.3389/fimmu.2021.602130
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suck abstract from ncbi


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pmid33746948      Front+Immunol 2021 ; 12 (ä): 602130
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  • Lung Protection vs Infection Resolution: Interleukin 10 Suspected of Double-Dealing in COVID-19 #MMPMID33746948
  • Lindner HA; Velasquez SY; Thiel M; Kirschning T
  • Front Immunol 2021[]; 12 (ä): 602130 PMID33746948show ga
  • The pathological processes by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection that make the virus a major threat to global health are insufficiently understood. Inefficient viral clearance at any stage is a hallmark of coronavirus disease 2019 (COVID-19). Disease severity is associated with increases in peripheral blood cytokines among which interleukin 10 (IL-10) increases particularly early and independent of patient age, which is not seen in active SARS-CoV infection. Here, we consider the known multi-faceted immune regulatory role of IL-10, both in protecting the lung from injury and in defense against infections, as well as its potential cellular source. While the absence of an IL-10 response in SARS is thought to contribute to early deterioration, we suspect IL-10 to protect the lung from early immune-mediated damage and to interfere with viral clearance in COVID-19. This may further both viral spread and poor outcome in many high-risk patients. Identifying the features of the viral genotype, which specifically underlie the different IL-10 dynamics as an etiological endotype and the different viral load kinetics and outcomes as clinical phenotype, may unveil a new immune evasive strategy of SARS-CoV-2.
  • |*Severity of Illness Index[MESH]
  • |Adult[MESH]
  • |Animals[MESH]
  • |COVID-19 Vaccines/immunology[MESH]
  • |COVID-19/*blood/*immunology/transmission/virology[MESH]
  • |Child[MESH]
  • |Genotype[MESH]
  • |Humans[MESH]
  • |Interleukin-10/*blood[MESH]
  • |Lung/*immunology/*pathology[MESH]
  • |Mice[MESH]
  • |Phenotype[MESH]
  • |SARS-CoV-2/*genetics/immunology[MESH]


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