They recognize pathogen-associated molecular patterns (PAMPs) that are expressed on infectious agents, and mediate the production of cytokines necessary for the development of effective immunity.

Although not yet fully elucidated, using an unbiased genome-scale screen with short hairpin RNA (shRNA), it has been demonstrated that the receptor TREML4 acts as an essential positive regulator of TLR7 signaling.

TREML4 deficiency reduced the production of inflammatory cytokines and autoantibodies in MRL/lpr mice, suggesting that TLR7 is a vital component of antiviral immunity and a predecessor factor in the pathogenesis of rheumatic diseases such as systemic lupus erythematosus (SLE).

[18] These findings suggest that TLR7 not only plays a key role in triggering the immune response against COVID-19 but may also mediate the post-infectious sequalae in critically ill patients.

[18] Further research is required to fully delineate the mechanisms by which functional impairment of TLR7 influences the disease process and to explore the potential efficacy of targeting this pathway in the treatment of COVID-19.