The leukocyte immunoglobulin-like receptor A3 (LILRA3) is a soluble immune receptor belonging to the LILR family, which regulates innate and adaptive immune responses. Unlike most LILRs, LILRA3 lacks transmembrane and cytoplasmic domains, existing primarily as a secreted protein. It is encoded by a polymorphic gene located within the leukocyte receptor complex on chromosome 19q13.4. LILRA3 binds to MHC class I molecules and other ligands, modulating immune cell activation, cytokine production, and antigen presentation. Its expression is restricted to myeloid cells, such as monocytes and dendritic cells, though levels vary across individuals due to genetic polymorphisms or deletions.
LILRA3 has been implicated in autoimmune and inflammatory diseases. Reduced LILRA3 expression or genetic deletion is associated with increased susceptibility to rheumatoid arthritis, multiple sclerosis, and systemic lupus erythematosus, potentially due to dysregulated immune inhibition. Conversely, elevated LILRA3 levels are observed in chronic viral infections, suggesting a role in immune evasion.
Anti-LILRA3 antibodies are research tools used to detect LILRA3 in biological samples, study its interactions with ligands, and explore its functional roles in disease models. These antibodies aid in understanding how LILRA3 variants influence immune homeostasis and pathogenesis, offering insights for therapeutic targeting in immune-related disorders.