Tlr6, a member of the Toll-like receptor family, is a type-I transmembrane receptor with an extracellular leucine-rich repeat (LRR) domain and a cytoplasmic Toll/IL-1 receptor-like region [6]. It plays a crucial role in the innate immune response by recognizing conserved microbial products, such as peptidoglycan from Gram-positive bacteria. TLR6 often forms heterodimers with TLR2 to activate the signaling cascade, leading to the activation of multiple inflammatory genes and thus regulating both innate and adaptive immunity [3].

In terms of disease-related findings, the TLR2/TLR6 ligand FSL-1 was shown to mitigate radiation-induced hematopoietic injury in mice and non-human primates, promoting hematopoietic progenitor cell proliferation and red blood cell development [1]. High TLR6 expression status in locally advanced thoracic esophageal squamous cell carcinoma patients predicted a more favorable prognosis after esophagectomy, and peptidoglycan (recognized by TLR6) inhibited the cell proliferation activity of esophageal squamous cell carcinoma lines [2]. In sepsis-induced ARDS, miR-34a-5p may promote TLR6 to heighten inflammation [4]. Also, sustained exposure to Helicobacter pylori desensitized TLR6, inducing immune tolerance, and restoration of TLR6 reduced H. pylori colonization in gerbils [5].

In conclusion, Tlr6 is essential for innate immunity and has significant implications in various disease conditions. Studies using animal models, like the non-human primates and gerbils in the above-mentioned research, have revealed its role in radiation-induced hematopoietic injury, cancer prognosis, and infectious disease-related immune responses. Understanding Tlr6 function provides potential therapeutic targets for these diseases.