Leukocyte immunoglobulin-like receptor A2 (LILRA2) is an activating receptor belonging to the LILR family, primarily expressed on myeloid cells such as monocytes, macrophages, and dendritic cells. It contains immunoglobulin-like extracellular domains but lacks canonical signaling motifs, instead associating with adaptor proteins (e.g., FcRγ) to mediate immune activation. LILRA2 binds pathogen-associated molecules and endogenous ligands, modulating inflammatory responses and antigen presentation. Its dysregulation is implicated in autoimmune diseases (e.g., rheumatoid arthritis, multiple sclerosis) and infectious diseases (e.g., HIV, tuberculosis), where altered receptor expression correlates with disease severity or immune evasion.
LILRA2-specific antibodies are critical research tools for investigating receptor-ligand interactions, signaling pathways, and pathological mechanisms. Monoclonal antibodies targeting LILRA2 have shown potential in preclinical studies to block pro-inflammatory signaling or enhance anti-pathogen immunity. However, challenges remain due to LILRA2's genetic polymorphism, which affects ligand binding and antibody specificity across populations. Additionally, its overlapping functions with other LILRs and heterogeneity in myeloid cell subsets complicate therapeutic targeting. Current research focuses on developing high-affinity antibodies with clinical utility while elucidating LILRA2's dual roles in immune homeostasis and disease progression.