TLRs in COVID-19: How they drive immunopathology and the rationale for modulation. Issue 7 (October 2021)

• Record Type: Journal Article
• Authors: Mabrey, F. Linzee; Morrell, Eric D; Wurfel, Mark M
• Is Part Of: Innate immunity. Volume 27:Issue 7/8(2021)
• Page Start: 503
• Page End: 513
• Publication Date: 2021-10
• Subjects: TLR -- COVID-19 -- innate immunity -- interferon -- CD14; Natural immunity -- Periodicals; Endotoxins -- Periodicals; 616.07905
• DOI: 10.1177/17534259211051364
• Languages: English
• ISSNs: 1753-4259

Abstract

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.