Leukocyte immunoglobulin-like receptor subfamily B member 2 (LILRB2) (LILRB2)

Leukocyte immunoglobulin-like receptor subfamily B member 2 (LILRB2), also known as ILT4, is a type I transmembrane inhibitory receptor predominantly expressed on myeloid lineage cells, including monocytes, macrophages, and dendritic cells [1, 2]. It belongs to the immunoglobulin superfamily and functions by transmitting suppressive signals through its cytoplasmic immunoreceptor tyrosine-based inhibitory motifs (ITIMs), which recruit phosphatases like SHP-1 and SHP-2 [1, 6]. In the tumor microenvironment, LILRB2 acts as a critical myeloid checkpoint; its interaction with ligands such as MHC class I molecules (notably HLA-G) promotes the polarization of tumor-associated macrophages toward an immunosuppressive M2-like phenotype, thereby facilitating immune evasion [6, 11, 12]. Beyond its role in oncology, LILRB2 has been identified as a high-affinity receptor for beta-amyloid oligomers in the central nervous system, where it mediates synaptic plasticity deficits and neurodegeneration in Alzheimer's disease [1, 10]. Therapeutic development is primarily focused on antagonistic monoclonal antibodies designed to block these inhibitory interactions, thereby "reprogramming" the immune environment to favor anti-tumor activity or potentially mitigating neurotoxic signaling in neurodegenerative conditions [12, 15, 16].

Other names

ILT4CD85dLIR2MIR10Immunoglobulin-like transcript 4Leukocyte immunoglobulin-like receptor 2Monocyte/macrophage immunoglobulin-like receptor 10

Antagonist; Immune checkpoint inhibition; Myeloid cell reprogramming; Macrophage repolarization (M2 to M1) [2, 6, 12, 13].