LILRA4

Leukocyte immunoglobulin-like receptor subfamily A member 4 (LILRA4), also termed ILT7 or CD85g, is an inhibitory receptor predominantly expressed on plasmacytoid dendritic cells (pDCs). It binds to extracellular nucleic acids via association with the FcεRIγ chain, suppressing excessive type I interferon (IFN-α/β) production through SYK-mediated signaling pathways. LILRA4 modulates TLR7/9-driven antiviral responses and maintains immune tolerance by negatively regulating autoreactive B-cell activation. Dysregulation of LILRA4 is implicated in autoimmune disorders such as systemic lupus erythematosus (SLE), where reduced receptor expression correlates with hyperactive IFN signatures. In oncology, LILRA4-mediated immunosuppression may facilitate tumor immune evasion. Therapeutic strategies targeting LILRA4 include antagonistic monoclonal antibodies (e.g., MK-0482) in early-phase trials for autoimmune diseases and IFN-driven malignancies, while agonists are explored for enhancing antiviral immunity in chronic infections.