Leukocyte immunoglobulin-like receptor subfamily A member 3 (LILRA3)

Leukocyte immunoglobulin-like receptor subfamily A member 3 (LILRA3) is a soluble immune regulatory protein encoded by the LILRA3 gene on chromosome 19q13.4[2][3][4][5]. Unlike other LILR family members, LILRA3 lacks a transmembrane domain and is secreted, not membrane-bound[2][3][4]. LILRA3 is primarily produced by monocytes and macrophages, possibly B cells, and can bind classical and non-classical HLA class I molecules, though with lower affinity than membrane-bound family members LILRB1 and LILRB2[1][2][5]. Through its molecular homology, it may modulate immune reactions by acting as a soluble competitor to membrane-bound LILR–HLA interactions, potentially influencing susceptibility to autoimmune diseases and playing a role in inflammation, immune cell differentiation, and cytokine regulation[3][4][6]. LILRA3 is highly polymorphic: a 6.7-kb gene deletion variant is common in some populations, leading to loss of protein expression and influencing individual disease risk[3][4][6]. Serum LILRA3 concentrations have been identified as a potential biomarker for disease severity in multiple sclerosis[4]. No direct drug interactions are currently documented, and the physiologic and therapeutic roles of LILRA3 are still being elucidated.

Other names

CD85eimmunoglobulin-like transcript 6 (ILT-6)leukocyte immunoglobulin-like receptor 4 (LIR-4)CD85 antigen-like family member E

Putative soluble antagonist/agonist modulating LILR–HLA-I interactions; Inhibition of LPS-mediated TNFα production in monocytes