Tlr1, Toll-like receptor 1, is a key component in the innate immune system. It often forms heterodimers with Tlr2 and recognizes various microbial ligands, especially bacterial lipoproteins. This recognition activates signaling cascades such as the MAPK and NF-κB pathways, playing a crucial role in initiating immune responses against pathogens [2,3].

Lactobacillus johnsonii, a potential anti-inflammatory bacterium, can alleviate colitis through the Tlr1/2-STAT3 mediated activation of CD206+ macrophages-IL-10. Tlr1/2 is essential for the activation of STAT3 and the recognition of L. johnsonii by macrophages, suggesting its role in modulating gut microbiota-related immune responses in ulcerative colitis [1]. In hybrid yellow catfish, the expression of Tlr1 is up-regulated after Aeromonas hydrophila stimulation, indicating its participation in the inflammatory response to exogenous pathogen infection [4].

In conclusion, Tlr1 is vital for the innate immune response, recognizing microbial ligands and activating relevant signaling pathways. Its role in diseases like ulcerative colitis and in response to pathogen infections in fish has been revealed through in vivo studies, highlighting its significance in understanding immune-related disease mechanisms and potentially developing new therapeutic strategies.