Cd300lf, a gene encoding an inhibitory immunoreceptor, is involved in multiple biological functions. It binds to ligands like ceramide and phosphatidylserine, and is associated with regulating immune responses and cell-virus interactions. Genetic models, such as gene knockout and conditional knockout mouse models, have been crucial for studying its functions [4].

In Cd300lf-deficient mice, an increase in glial cell proliferation, extensive neuronal loss, and worsened neurological function were observed post-traumatic brain injury (TBI), indicating that Cd300lf reduces neuroinflammation and promotes neurological recovery after TBI by inhibiting the STING signaling pathway [1]. A Cd300lf conditional knockout (CD300lfF/F) mouse model revealed that CD300lf expression on intestinal epithelial cells, especially tuft cells, is essential for the transmission of the persistent murine norovirus (MNoV) strain CR6, while the non-persistent MNoV strain CW3 has a different cell tropism and partially relies on CD300lf-expressing myelomonocytic cells [2]. Ablation of Cd300lf in a ligature-induced periodontitis model increased the number of osteoclasts and exacerbated bone damage, suggesting that the interaction of CD300lf and ceramide reduces the development of periodontitis by inhibiting osteoclast differentiation [3].

In conclusion, Cd300lf plays essential roles in regulating neuroinflammation after TBI, norovirus cell tropism, and osteoclast-related periodontitis. The Cd300lf KO/CKO mouse models have significantly contributed to understanding its functions in these disease-related biological processes, providing potential therapeutic targets for TBI, norovirus-related infections, and periodontitis.