Cd300lf, also known as myeloid-associated Ig-like receptor V (MAIR-V), is an inhibitory immunoreceptor. It plays crucial roles in multiple biological processes, including regulation of cell activation and viral infection. It has been associated with the regulation of innate immune responses and interacts with ligands like ceramide and phosphatidylserine. Genetic models, such as knockout (KO) and conditional knockout (CKO) mouse models, have been instrumental in studying its functions [1,2,3,4,5,6,7,8].

In Cd300lf-deficient mice, after traumatic brain injury (TBI), there was increased glial cell proliferation, more extensive neuronal loss, and worsened neurological function, indicating that Cd300lf reduces neuroinflammation and promotes neurological recovery after TBI by inhibiting the STING signaling pathway [1]. In the context of murine norovirus (MNoV) infection, a Cd300lf conditional knockout mouse model demonstrated that Cd300lf expression on intestinal epithelial cells, especially tuft cells, is essential for transmission of the persistent MNoV strain CR6, while myelomonocytic cells are a major target for the non-persistent MNoVCW3 strain [2]. Ablation of Cd300lf in a ligature-induced periodontitis model increased the number of osteoclasts and exacerbated bone damage, suggesting its role in inhibiting osteoclast differentiation and alveolar bone loss in periodontitis [3].

In conclusion, Cd300lf has diverse functions in different biological processes and disease conditions. KO/CKO mouse models have been crucial in revealing its roles in TBI, MNoV-related pathogenesis, and periodontitis, highlighting its potential as a therapeutic target in these disease areas.