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10.1177/17534259211051364

http://scihub22266oqcxt.onion/10.1177/17534259211051364
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34806446!8762091!34806446
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suck abstract from ncbi


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pmid34806446      Innate+Immun 2021 ; 27 (7-8): 503-513
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  • TLRs in COVID-19: How they drive immunopathology and the rationale for modulation #MMPMID34806446
  • Mabrey FL; Morrell ED; Wurfel MM
  • Innate Immun 2021[Oct]; 27 (7-8): 503-513 PMID34806446show ga
  • COVID-19 is both a viral illness and a disease of immunopathology. Proximal events within the innate immune system drive the balance between deleterious inflammation and viral clearance. We hypothesize that a divergence between the generation of excessive inflammation through over activation of the TLR associated myeloid differentiation primary response (MyD88) pathway relative to the TIR-domain-containing adaptor-inducing IFN-beta (TRIF) pathway plays a key role in COVID-19 severity. Both viral elements and damage associated host molecules act as TLR ligands in this process. In this review, we detail the mechanism for this imbalance in COVID-19 based on available evidence, and we discuss how modulation of critical elements may be important in reducing severity of disease.
  • |Animals[MESH]
  • |COVID-19/immunology/*metabolism/*pathology[MESH]
  • |Humans[MESH]
  • |Immunity, Innate[MESH]
  • |Signal Transduction/drug effects[MESH]


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