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...
| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
| Published: |
SAGE Publishing
2021-10-01
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| Series: | Innate Immunity |
| Online Access: | https://doi.org/10.1177/17534259211051364 |
| _version_ | 1797936117107916800 |
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| 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 |
| collection | DOAJ |
| 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. |
| first_indexed | 2024-04-10T18:25:43Z |
| format | Article |
| id | doaj.art-974427168b5e4e37bfe9dcaa25899ffa |
| institution | Directory Open Access Journal |
| issn | 1753-4259 1753-4267 |
| language | English |
| last_indexed | 2024-04-10T18:25:43Z |
| publishDate | 2021-10-01 |
| publisher | SAGE Publishing |
| record_format | Article |
| series | Innate Immunity |
| spelling | doaj.art-974427168b5e4e37bfe9dcaa25899ffa2023-02-02T06:03:24ZengSAGE PublishingInnate Immunity1753-42591753-42672021-10-012710.1177/17534259211051364TLRs in COVID-19: How they drive immunopathology and the rationale for modulationF. Linzee MabreyEric D MorrellMark M WurfelCOVID-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.https://doi.org/10.1177/17534259211051364 |
| spellingShingle | F. Linzee Mabrey Eric D Morrell Mark M Wurfel TLRs in COVID-19: How they drive immunopathology and the rationale for modulation Innate Immunity |
| title | 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_short | 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 |
| url | https://doi.org/10.1177/17534259211051364 |
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