{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nLILRA3 is a unique member of the leukocyte immunoglobulin‐like receptor family because it is secreted rather than membrane bound. Structural and sequence‐based studies have revealed that LILRA3 lacks transmembrane and cytoplasmic domains, and that several polymorphic residues in its immunoglobulin‐like domains likely affect its ligand‐binding properties. Indeed, biochemical analyses indicate that, unlike other LILRs that bind folded HLA class I molecules, LILRA3 preferentially interacts with free heavy chain (for example, HLA‐C free chains) and shows overall reduced binding affinity relative to its membrane‐bound homologues."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": "\n\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFunctionally, LILRA3 appears to play an important role in modulating immune responses. Several genetic studies have linked the presence or deletion of the LILRA3 gene with susceptibility to autoimmune and inflammatory disorders. For example, loss‐of‐function alleles or homozygous deletions are associated with higher incidence and an earlier onset of diseases such as multiple sclerosis, Sjögren’s syndrome, and rheumatoid arthritis. In vitro analyses demonstrate that exogenous LILRA3 can bind to monocytes and B cells, triggering the secretion of cytokines and stimulating proliferation of cytotoxic lymphocytes (including CD8⁺ T cells and natural killer cells). By acting as a competitive agonist/antagonist relative to activating LILR receptors, LILRA3 helps to balance activating and inhibitory immune signals."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "16"}]}, {"type": "t", "text": "\n\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its immunomodulatory role in autoimmunity, LILRA3 has been implicated in a variety of other pathological contexts. In neuroimmunology, soluble LILRA3 binds with high affinity to Nogo‐66—a myelin‐associated inhibitor—and by doing so it antagonizes inhibitory signaling, thereby promoting neurite outgrowth and synaptogenesis through the ERK/MEK pathway. In addition, altered LILRA3 expression is linked not only to multiple sclerosis severity but also to conditions with inflammatory components such as benign prostatic hyperplasia, nasopharyngeal carcinoma, and antiphospholipid syndrome. Its modulatory actions also extend to infectious diseases where LILRA3 regulation appears to influence cytotoxic cell proliferation in HIV infection. Moreover, over‐expression studies in monocytes have shown that LILRA3 can dampen the secretion of pro‐inflammatory cytokines while enhancing phagocytosis and cell proliferation via Akt and Erk/MEK pathways, as seen in inflammatory bowel disease. Finally, genetic interactions with other loci—including those in Takayasu arteritis and systemic lupus erythematosus—underscore the broader importance of LILRA3 in regulating inflammatory and immune homeostasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "29"}]}, {"type": "t", "text": "\n\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "S J Moodie, P J Norman, A L King, et al. 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