Clec12a, also known as CD301b, is a C-type lectin receptor. It is involved in innate immune surveillance, regulating immune responses, and is associated with pathways related to inflammation and phagocytosis. Its expression in different cell types like macrophages, dendritic cells, and neutrophils is crucial for maintaining immune balance [1,2,3,4].

In mice, Clec12a -/- mice developed severe colitis dependent on the microbiota, with expansion of Faecalibaculum rodentium. Macrophages in the gut of these KO mice showed heightened inflammation and reduced phagocytosis-related genes, indicating Clec12a's role in tempering inflammation and restricting the expansion of colitogenic commensals [2]. Also, Clec12a was found to inhibit monosodium uric acid (MSU)-induced immune activation in a mechanism that disrupts MSU-induced lipid raft recruitment, highlighting its role in controlling solid particle-induced immune activation [3].

In conclusion, Clec12a is essential for innate immune regulation, playing a role in controlling inflammation, phagocytosis, and immune responses to certain pathogens and particles. The gene knockout mouse models have been instrumental in revealing its functions in colitis and MSU-induced immune activation, providing insights into potential therapeutic targets for related diseases.