TLRs in COVID-19: How they drive immunopathology and the rationale for modulation
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...
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SAGE Publishing
2021
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oai:doaj.org-article:974427168b5e4e37bfe9dcaa25899ffa2021-12-02T07:35:13ZTLRs in COVID-19: How they drive immunopathology and the rationale for modulation1753-42591753-426710.1177/17534259211051364https://doaj.org/article/974427168b5e4e37bfe9dcaa25899ffa2021-10-01T00:00:00Zhttps://doi.org/10.1177/17534259211051364https://doaj.org/toc/1753-4259https://doaj.org/toc/1753-4267COVID-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-β (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.F. Linzee MabreyEric D MorrellMark M WurfelSAGE PublishingarticleImmunologic diseases. AllergyRC581-607ENInnate Immunity, Vol 27 (2021) |
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DOAJ |
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EN |
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Immunologic diseases. Allergy RC581-607 |
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Immunologic diseases. Allergy RC581-607 F. Linzee Mabrey Eric D Morrell Mark M Wurfel TLRs in COVID-19: How they drive immunopathology and the rationale for modulation |
description |
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-β (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. |
format |
article |
author |
F. Linzee Mabrey Eric D Morrell Mark M Wurfel |
author_facet |
F. Linzee Mabrey Eric D Morrell Mark M Wurfel |
author_sort |
F. Linzee Mabrey |
title |
TLRs in COVID-19: How they drive immunopathology and the rationale for modulation |
title_short |
TLRs in COVID-19: How they drive immunopathology and the rationale for modulation |
title_full |
TLRs in COVID-19: How they drive immunopathology and the rationale for modulation |
title_fullStr |
TLRs in COVID-19: How they drive immunopathology and the rationale for modulation |
title_full_unstemmed |
TLRs in COVID-19: How they drive immunopathology and the rationale for modulation |
title_sort |
tlrs in covid-19: how they drive immunopathology and the rationale for modulation |
publisher |
SAGE Publishing |
publishDate |
2021 |
url |
https://doaj.org/article/974427168b5e4e37bfe9dcaa25899ffa |
work_keys_str_mv |
AT flinzeemabrey tlrsincovid19howtheydriveimmunopathologyandtherationaleformodulation AT ericdmorrell tlrsincovid19howtheydriveimmunopathologyandtherationaleformodulation AT markmwurfel tlrsincovid19howtheydriveimmunopathologyandtherationaleformodulation |
_version_ |
1718399351744626688 |