CLEC12A (C-type lectin domain family 12 member A), also known as MICL or DCAL-2. is a transmembrane protein belonging to the C-type lectin receptor (CLR) family. It is primarily expressed on myeloid cells, including monocytes, neutrophils, and dendritic cells, as well as on certain malignant cells, such as acute myeloid leukemia (AML) blasts. Structurally, CLEC12A contains an extracellular C-type lectin-like domain, a transmembrane region, and a cytoplasmic immunoreceptor tyrosine-based inhibitory motif (ITIM). As an inhibitory receptor, it regulates immune responses by dampening activation signals, thereby maintaining immune homeostasis and preventing excessive inflammation.
CLEC12A antibodies target this receptor for both diagnostic and therapeutic purposes. In research, these antibodies are used to study CLEC12A's role in immune regulation, myeloid cell differentiation, and tumor immune evasion. Clinically, CLEC12A is considered a promising biomarker and therapeutic target in AML due to its high expression on leukemic cells and limited presence on healthy tissues. Antibody-based therapies, such as antibody-drug conjugates (ADCs) or CAR-T cell therapies, leverage CLEC12A antibodies to selectively eliminate malignant cells while sparing normal cells. Additionally, CLEC12A antibodies are employed in flow cytometry and immunohistochemistry to identify and characterize myeloid malignancies. Despite its immunosuppressive function in normal physiology, CLEC12A’s aberrant expression in cancers highlights its dual role as a regulator and a disease-associated antigen, driving ongoing research into its therapeutic potential.