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The deregulated immune reaction and cytokines release storm (CRS) in COVID-19 disease

COVID-19 caused by the SARS-CoV-2 virus, accompanies an unprecedented spike in cytokines levels termed cytokines release syndrome (CRS), in critically ill patients. Clinicians claim that the surge demonstrates a deregulated immune defence in host, as infected cell expression analysis depicts a delay...

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Detalles Bibliográficos
Autores principales: Pasrija, Ritu, Naime, Mohammad
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier B.V. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7691139/
https://www.ncbi.nlm.nih.gov/pubmed/33302033
http://dx.doi.org/10.1016/j.intimp.2020.107225
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author Pasrija, Ritu
Naime, Mohammad
author_facet Pasrija, Ritu
Naime, Mohammad
author_sort Pasrija, Ritu
collection PubMed
description COVID-19 caused by the SARS-CoV-2 virus, accompanies an unprecedented spike in cytokines levels termed cytokines release syndrome (CRS), in critically ill patients. Clinicians claim that the surge demonstrates a deregulated immune defence in host, as infected cell expression analysis depicts a delay in type-I (interferon-I) and type-III IFNs expression, along with a limited Interferon-Stimulated Gene (ISG) response, which later resume and culminates in elicitation of several cytokines including- IL-6, IL-8, IL-12, TNFα, IL-17, MCP-1, IP-10 and IL-10 etc. Although cytokines are messenger molecules of the immune system, but their increased concentration results in inflammation, infiltration of macrophages, neutrophils and lung injury in patients. This inflammatory response results in the precarious pathogenesis of COVID-19; thus, a complete estimation of the immune response against SARS-CoV-2 is vital in designing a harmless and effective vaccine. In pathogenesis analysis, it emerges that a timely forceful type-I IFN production (18–24 hrs post infection) promotes innate and acquired immune responses, while a delay in IFNs production (3–4 days post infection) actually renders both innate and acquired responses ineffective in fighting infection. Further, underlying conditions including hypertension, obesity, cardio-vascular disease etc may increase the chances of putting people in risk groups, which end up having critical form of infection. This review summarizes the events starting from viral entry, its struggle with the immune system and failure of host immunological parameters to obliterate the infections, which finally culminate into massive release of CRS and inflammation in gravely ill patients.
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spelling pubmed-76911392020-11-27 The deregulated immune reaction and cytokines release storm (CRS) in COVID-19 disease Pasrija, Ritu Naime, Mohammad Int Immunopharmacol Review COVID-19 caused by the SARS-CoV-2 virus, accompanies an unprecedented spike in cytokines levels termed cytokines release syndrome (CRS), in critically ill patients. Clinicians claim that the surge demonstrates a deregulated immune defence in host, as infected cell expression analysis depicts a delay in type-I (interferon-I) and type-III IFNs expression, along with a limited Interferon-Stimulated Gene (ISG) response, which later resume and culminates in elicitation of several cytokines including- IL-6, IL-8, IL-12, TNFα, IL-17, MCP-1, IP-10 and IL-10 etc. Although cytokines are messenger molecules of the immune system, but their increased concentration results in inflammation, infiltration of macrophages, neutrophils and lung injury in patients. This inflammatory response results in the precarious pathogenesis of COVID-19; thus, a complete estimation of the immune response against SARS-CoV-2 is vital in designing a harmless and effective vaccine. In pathogenesis analysis, it emerges that a timely forceful type-I IFN production (18–24 hrs post infection) promotes innate and acquired immune responses, while a delay in IFNs production (3–4 days post infection) actually renders both innate and acquired responses ineffective in fighting infection. Further, underlying conditions including hypertension, obesity, cardio-vascular disease etc may increase the chances of putting people in risk groups, which end up having critical form of infection. This review summarizes the events starting from viral entry, its struggle with the immune system and failure of host immunological parameters to obliterate the infections, which finally culminate into massive release of CRS and inflammation in gravely ill patients. Elsevier B.V. 2021-01 2020-11-27 /pmc/articles/PMC7691139/ /pubmed/33302033 http://dx.doi.org/10.1016/j.intimp.2020.107225 Text en © 2020 Elsevier B.V. All rights reserved. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.
spellingShingle Review
Pasrija, Ritu
Naime, Mohammad
The deregulated immune reaction and cytokines release storm (CRS) in COVID-19 disease
title The deregulated immune reaction and cytokines release storm (CRS) in COVID-19 disease
title_full The deregulated immune reaction and cytokines release storm (CRS) in COVID-19 disease
title_fullStr The deregulated immune reaction and cytokines release storm (CRS) in COVID-19 disease
title_full_unstemmed The deregulated immune reaction and cytokines release storm (CRS) in COVID-19 disease
title_short The deregulated immune reaction and cytokines release storm (CRS) in COVID-19 disease
title_sort deregulated immune reaction and cytokines release storm (crs) in covid-19 disease
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7691139/
https://www.ncbi.nlm.nih.gov/pubmed/33302033
http://dx.doi.org/10.1016/j.intimp.2020.107225
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