Clec1b, also known as the gene encoding the CLEC-2 protein, is a member of the C-type lectin superfamily. It is a type II transmembrane receptor involved in platelet activation, angiogenesis, immune and inflammatory responses, tumor cell metastasis, separation of blood/lymphatic vessels, and cerebrovascular patterning during embryonic development [1,2,3]. It binds to ligands like podoplanin and is expressed on platelets, Kupffer cells, and other immune cells [3].

Using constitutive Clec1b(-/-) mice, it was shown that CLEC-2 was not necessary for initiation of the lymph node anlage but required at late stages of development. Constitutive deletion induced a profound defect in lymphatic endothelial cell proliferation, resulting in lack of lymph nodes at birth. Conditional deletion of CLEC-2 in the megakaryocyte/platelet lineage in Clec1b(fl/fl)PF4-Cre mice led to the development of blood-filled lymph nodes and fibrosis, indicating CLEC-2 expression in platelets was required for lymph node integrity [4].

In conclusion, Clec1b plays essential roles in multiple biological processes. Its function in platelet-related processes and lymph node development has been well-demonstrated through gene knockout mouse models. Additionally, studies in hepatocellular carcinoma suggest its potential as a prognostic biomarker and immunoregulator, highlighting its significance in disease-related research [1-3, 9].