Virus in the pathogenesis of inflammatory bowel disease: role of Tolllike receptor 7/8/3

Inflammatory bowel disease (IBD) pathogenesis is influenced by immune system malfunction, particularly innate immune receptors such toll-like receptors. Furthermore, due to the extreme close association between viruses and IBD incidence, it is critical to further investigation between the virus and IBD. TLRs 3, 5, and 7 are three members of TLRs family that are involved in antiviral immune responses. Finding a relationship between TLR related virus and IBD is important not only for disease pathogenesis but also for therapeutic effectiveness. Furthermore, it has been shown that influenza expresses severe in patients with IBD who use immune system inhibitors, and the influenza vaccine is less effective in these patients. In dendritic cells, TLR7 and TLR8 regulate the production of interferons (IFNs) and inflammatory mediators. COVID-19 causes the production of IL-6, which could be due to the induction of TLR pathways. TLR activation by SARS-CoV-2 causes inflammation and IL-1 production, which induces IL-6 to be produced. Understanding the TLR associated viruses’ molecular mechanism can greatly help improve the quality of life of people with IBD. Therefore, the present study aimed to review the role of TLR7, 8 and 3 in inflammatory bowel disease, their association with viral infections and to evaluate different antagonists for the treatment of IBD.