Leukocyte immunoglobulin-like receptor subfamily B member 4 (for ILT3); Leukocyte immunoglobulin-like receptor subfamily B member 2 (for ILT4) (ILT3 (for LILRB4), ILT4 (for LILRB2))

ILT3 (LILRB4): Leukocyte immunoglobulin-like receptor subfamily B member 4 is an inhibitory immune receptor predominantly expressed on myeloid cells, including monocytes and dendritic cells[2][3][5]. It contains immunoreceptor tyrosine-based inhibitory motifs (ITIMs) in its cytoplasmic domain, transmitting inhibitory signals that promote immune tolerance and suppress T-cell and natural killer (NK) cell activation[2][3]. High expression of ILT3 is associated with tolerogenic dendritic cells, immune escape in the tumor microenvironment, and impaired antitumor immunity[2][5]. ILT3 modulates immune suppression through interaction with the extracellular matrix protein fibronectin, which polarizes myeloid cells toward a suppressive state; this can be reversed with anti-ILT3 antibodies[2]. It is a therapeutic target in immuno-oncology, with several antibody therapies in development[2][5]. ILT4 (LILRB2): Leukocyte immunoglobulin-like receptor subfamily B member 2 is an inhibitory receptor also found on myeloid cells, especially dendritic cells and monocytes[7][8]. ILT4 interacts with HLA-G and other MHC class I molecules, negatively regulating immune activation and contributing to immune tolerance, transplant acceptance, and tumor immune evasion[4][7][8]. Like ILT3, it is implicated in tumor immune escape and is a target of antibodies aimed at reversing immune suppression[7][8]. Note: ILT3 and ILT4 are distinct but related proteins; their functions, expression, and disease associations partially overlap but are not identical.

Other names

LILRB4CD85kLIR-5LILRB2CD85dLIR-2

Blockade of immune inhibitory signaling (via antibody binding) - Reversal of myeloid-derived suppressor cell polarization (for ILT3)[2][5] - Enhancement of T cell activation and reversal of immune tolerance