C-type lectin domain family 2 member A (CLEC2A)

C-type lectin domain family 2 member A (CLEC2A), also known as KACL (Keratinocyte-associated C-type lectin) or PILAR (Proliferation-induced lymphocyte-associated receptor), is a receptor encoded by the NKC (natural killer gene complex) and is a member of the C-type lectin-like receptor family[1][2][3][4][5]. CLEC2A is predominantly expressed on keratinocytes in human skin, with minimal or absent expression in peripheral blood mononuclear cells and other tissues[2][4][6]. Structurally, it is a non–disulfide-linked homodimeric surface receptor, functioning as a ligand for the activating receptor NKp65/KLRF2 on natural killer (NK) cells[2][4][6]. This interaction facilitates immunosurveillance of human skin by stimulating NK cell-mediated cytotoxicity and promoting release of proinflammatory cytokines, thus playing a role in cutaneous immune defense and possibly skin pathology[1][2][4][6]. CLEC2A also participates in processes such as T cell receptor signaling and regulation of interleukin-2 production[1][3]. Disease association includes rare skin tumors such as Pilar Sheath Acanthoma, and it may be relevant for skin-related immune diseases, though its clinical targeting and biomarker status remain unestablished[1][2][4][6].

Other names

KACLPILARUNQ5792PRO19597INPE5792Keratinocyte-associated C-type lectinProliferation-induced lymphocyte-associated receptor

Engagement by counterpart activating receptor (NKp65) stimulates NK cell cytotoxicity and cytokine secretion (receptor-ligand immune recognition)