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Coronaviruses: Innate Immunity, Inflammasome Activation, Inflammatory Cell Death, and Cytokines

Authors
  • Lee, SangJoon1
  • Channappanavar, Rudragouda2, 3
  • Kanneganti, Thirumala-Devi1
  • 1 Department of Immunology, St Jude Children's Research Hospital, Memphis, TN 38105, USA
  • 2 Department of Microbiology, Immunology, and Biochemistry, University of Tennessee Health Sciences Center, Memphis, TN 38163, USA
  • 3 Department of Acute and Tertiary Care, University of Tennessee Health Sciences Center, Memphis, TN 38163, USA
Type
Published Article
Journal
Trends in Immunology
Publisher
Elsevier Ltd.
Publication Date
Oct 15, 2020
Identifiers
DOI: 10.1016/j.it.2020.10.005
PMCID: PMC7561287
Source
PubMed Central
Keywords
License
Unknown

Abstract

Toll-like receptor (TLR)- and retinoic acid-inducible gene I-like receptor (RLR)-mediated type I interferon (IFN) production is essential for providing protection against coronavirus (CoV) infection; the timing of the IFN response relative to CoV replication determines infection outcomes. Optimal NLR family pyrin domain-containing 3 (NLRP3) inflammasome activation is beneficial for the host but aberrant activation may lead to detrimental CoV infection outcomes. Specific CoV infections can activate inflammatory cell death (PANoptosis), thereby inducing cytokine release. CoV disease tolerance occurs in age-, species-, and sex-dependent manners. More studies are needed to define the innate immune response, specifically during severe acute respiratory syndrome (SARS)-CoV-2 (SARS-CoV-2) infection, and to inform the development of candidate therapeutics.

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