<unk>  has been shown to play a significant role in the pathogenesis of autoimmune disorders such as lupus as well as in the regulation of antiviral 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<unk>  signaling. In TREML4 -/- mice macrophages that are hyporesponsive to<unk>  agonists, macrophages fail to produce type I interferons due to impaired phosphorylation of the transcription factor STAT1 by the mitogen-activated protein kinase p38 and decreased recruitment of the adaptor MYD88 to<unk> . TREML4 deficiency reduced the production of inflammatory cytokines and autoantibodies in MRL/lpr mice, suggesting that<unk>  is a vital component of antiviral immunity and a predecessor factor in the pathogenesis of rheumatic diseases such as systemic lupus erythematosus (SLE). A<unk>  agonist, imiquimod (Aldara), has been approved for topical use in treating warts caused by papillomavirus and for actinic keratosis. Due to their ability to induce robust production of anti-cancer cytokines such as interleukin-12,<unk>  agonists have been investigated for cancer immunotherapy. Recent examples include TMX-202 delivery via liposomal formulation, as well as the delivery of resiquimod via nanoparticles formed from beta-cyclodextrin. In July 2020, it was discovered that a deficient<unk>  gene caused several young patients to become seriously ill after being infected by SARS-CoV-2. This suggests that<unk>  plays a key role in triggering the immune response for patients of COVID-19. For more details on the biological mechanism and pathway, see " Type I Interferon Induction and Signaling During SARS-CoV-2 Infection" on WikiPathways.
Toll-like receptor 7
Type I cytokine receptor
Fc receptor-like molecule
Type II cytokine receptor
Thromboxane receptor
Interleukin-7 receptor
Fc receptor
Interleukin-3 receptor