| Description |
Isoform 1: Non-classical major histocompatibility class Ib molecule involved in immune regulatory processes at the maternal-fetal interface (PMID:23184984, PMID:29262349, PMID:19304799). In complex with B2M/beta-2 microglobulin binds a limited repertoire of nonamer self-peptides derived from intracellular proteins including histones and ribosomal proteins (PMID:7584149, PMID:8805247). Peptide-bound HLA-G-B2M complex acts as a ligand for inhibitory/activating KIR2DL4, LILRB1 and LILRB2 receptors on uterine immune cells to promote fetal development while maintaining maternal-fetal tolerance (PMID:23184984, PMID:29262349, PMID:16366734, PMID:19304799, PMID:20448110, PMID:27859042). Upon interaction with KIR2DL4 and LILRB1 receptors on decidual NK cells, it triggers NK cell senescence-associated secretory phenotype as a molecular switch to promote vascular remodeling and fetal growth in early pregnancy (PMID:23184984, PMID:29262349, PMID:16366734, PMID:19304799). Through interaction with KIR2DL4 receptor on decidual macrophages induces proinflammatory cytokine production mainly associated with tissue remodeling (PMID:19304799). Through interaction with LILRB2 receptor triggers differentiation of type 1 regulatory T cells and myeloid-derived suppressor cells, both of which actively maintain maternal-fetal tolerance (PMID:20448110, PMID:27859042). May play a role in balancing tolerance and antiviral-immunity at maternal-fetal interface by keeping in check the effector functions of NK, CD8+ T cells and B cells (PMID:10190900, PMID:11290782, PMID:24453251). Reprograms B cells toward an immune suppressive phenotype via LILRB1 (PMID:24453251). May induce immune activation/suppression via intercellular membrane transfer (trogocytosis), likely enabling interaction with KIR2DL4, which resides mostly in endosomes (PMID:20179272, PMID:26460007). Through interaction with the inhibitory receptor CD160 on endothelial cells may control angiogenesis in immune privileged sites (PMID:16809620). Isoform 2: Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PMID:11290782). Isoform 3: Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PMID:11290782). Isoform 4: Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PMID:11290782). Isoform 5: Non-classical major histocompatibility class Ib molecule involved in immune regulatory processes at the maternal-fetal interface (PMID:23184984, PMID:29262349, PMID:19304799). In complex with B2M/beta-2 microglobulin binds a limited repertoire of nonamer self-peptides derived from intracellular proteins including histones and ribosomal proteins (PMID:7584149, PMID:8805247). Peptide-bound HLA-G-B2M complex acts as a ligand for inhibitory/activating KIR2DL4, LILRB1 and LILRB2 receptors on uterine immune cells to promote fetal development while maintaining maternal-fetal tolerance (PMID:23184984, PMID:29262349, PMID:16366734, PMID:19304799, PMID:20448110). Upon interaction with KIR2DL4 and LILRB1 receptors on decidual NK cells, it triggers NK cell senescence-associated secretory phenotype as a molecular switch to promote vascular remodeling and fetal growth in early pregnancy (PMID:23184984, PMID:29262349, PMID:16366734, PMID:19304799). Through interaction with KIR2DL4 receptor on decidual macrophages induces proinflammatory cytokine production mainly associated with tissue remodeling (PMID:19304799). Through interaction with LILRB2 receptor triggers differentiation of type 1 regulatory T cells and myeloid-derived suppressor cells, both of which actively maintain maternal-fetal tolerance (PMID:20448110). Reprograms B cells toward an immune suppressive phenotype via LILRB1 (PMID:24453251). Isoform 6: Likely does not bind B2M and presents peptides. Isoform 7: Likely does not bind B2M and presents peptides. |
| Cellular localization
|
Endoplasmic Reticulum Membrane, Membrane, Single-Pass Type I Membrane, Early Endosome Membrane, Secreted, Membrane, Early Endosome, Filopodium Membrane |
