Abstract
C-type lectin-like receptor 2 (CLEC-2, also known as CLEC-1b) is expressed on platelets, Kupffer cells and other immune cells, and binds to various ligands including the mucin-like protein podoplanin (PDPN). The role of CLEC-2 in infection and immunity has become increasingly evident in recent years. CLEC-2 is involved in platelet activation, tumor cell metastasis, separation of blood/lymphatic vessels, and cerebrovascular patterning during embryonic development. In this review, we have discussed the role of CLEC-2 in thromboinflammation, and focused on the recent research.
Highlights
CLEC-2 (CLEC-1b) is a type II transmembrane receptor [1, 2] of the C-type lectin superfamily, which are characterized by one or more C-type lectin-like domains (CTLDs)
Recent studies have confirmed that CLEC-2 does not recognize soluble HIV-1 envelope protein (Env), and the results show that virion incorporation of podoplanin was required for efficient CLEC-2-dependent HIV-1 interactions with cell lines and platelets
Bender et al showed that antibody-mediated blockade of either Glycoprotein VI (GPVI) (JAQ1) or CLEC-2 (INU1) in mice down-regulated their expression and activity on the platelet surface, but did not affect bleeding, whereas simultaneous inactivation of both completely inhibited thrombus formation
Summary
CLEC-2 (CLEC-1b) is a type II transmembrane receptor [1, 2] of the C-type lectin superfamily, which are characterized by one or more C-type lectin-like domains (CTLDs). Podoplanin is a type I transmembrane glycoprotein [26] that mediates venous thrombosis [27], extravascular platelet activation and inflammation in atherosclerosis [27, 28], and wound repair [29] upon binding to CLEC-2. A recent study showed that the smooth muscle calcium binding protein S100A13 is a potential ligand of CLEC2, and activates platelets independent of podoplanin [32].
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