Human leukocyte immunoglobulin (Ig)-like receptors (LILR) (白细胞免疫球蛋白样受体 (LILR); 免疫球蛋白样转录物 (ILT))

Human Leukocyte Immunoglobulin (Ig)-like Receptors (LILR) constitute a family of 11 innate immune-modulatory receptors that are primarily expressed on lymphoid and myeloid cells. Structurally and functionally, they resemble Killer Cell Ig-like Receptors (KIR) expressed on Natural Killer (NK) cells and subsets of T lymphocytes.
LILR are classified into activating (LILRA) and inhibitory (LILRB) types based on the differences in their associated signaling transduction domains (D). The activating LILRA subtypes include LILRA1–A6, which are also known as LIR6, ILT1, ILT6, ILT7, ILT11, and ILT8, respectively. The inhibitory LILRB subtypes include LILRB1–B5, which are also known as ILT2, ILT4, ILT5, ILT3, and LIR8, respectively. Except for soluble LILRA3, LILRA primarily mediates immune activation, while LILRB1-5 mainly inhibit immune responses and mediate immune tolerance. LILRB can serve as immune checkpoint molecules.
Abnormal expression and function of LILR are associated with various pathological conditions, including immunodeficiency (infections and malignancies) and excessive immune responses (autoimmunity and allograft rejection)^[1][2][3].