Clec4e, also known as Mincle, is a C-type lectin domain family 4 member. It plays a role in the immune response and is involved in various pathways such as those related to host-pathogen interactions [4,5]. It has significance in biological processes like sterile inflammation and host defense against pathogens [1,5]. Genetic models, especially KO mouse models, are valuable for studying its functions.

In myocardial ischemia-reperfusion injury, loss of Clec4e signaling in KO mice led to reduced acute cardiac injury, neutrophil infiltration, and infarct size, with improved left ventricular structural and functional remodeling at 4-week follow-up. The early transcriptome of KO mice showed upregulation of transcripts involved in myocardial metabolism, radical scavenging, angiogenesis, and extracellular matrix organization, indicating its role in myocardial repair [1].

In the context of pulmonary tuberculosis, genetic variations in Clec4e, such as rs10841847, were associated with an increased risk of developing pulmonary tuberculosis in a Guinea-Bissau population [2], while in a northern Chinese population, variations at rs10841845 and rs10841847 were associated with increased individual protection against pulmonary tuberculosis [6].

In gastric cancer, Clec4e was significantly upregulated, and high expression was associated with poor prognosis. In vitro experiments showed that targeting Clec4e inhibited cancer cell migration and invasion [3].

In dendritic cell function against Candida albicans, the TLR2/CLEC4E signaling pathway was down-regulated in FAM21-cKO (conditional knockout) mice, making them more susceptible to the infection [4]. Also, in intestinal barrier disruption, Clec4e was essential for Enterococcus faecalis-induced trained immunity in bone-marrow-derived progenitors [7].

In conclusion, Clec4e is crucial in the immune response and various disease conditions. Gene knockout and conditional knockout mouse models have revealed its roles in myocardial repair after ischemia-reperfusion injury, susceptibility to pulmonary tuberculosis, gastric cancer progression, host defense against Candida albicans, and in the context of intestinal barrier disruption. These findings enhance our understanding of the biological functions of Clec4e and its potential as a therapeutic target in related diseases.