COMPARTMENTS

HLA-G [ENSP00000366024]

Soluble HLA class I histocompatibility antigen, alpha chain G; [Isoform 1]: Non-classical major histocompatibility class Ib molecule involved in immune regulatory processes at the maternal-fetal interface . In complex with B2M/beta-2 microglobulin binds a limited repertoire of nonamer self-peptides derived from intracellular proteins including histones and ribosomal proteins . 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 (PubMed:23184984, PubMed:29262349, PubMed:16366734, PubMed:19304799, PubMed:20448110, PubMed: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 . Through interaction with KIR2DL4 receptor on decidual macrophages induces proinflammatory cytokine production mainly associated with tissue remodeling . 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 . 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 . Reprograms B cells toward an immune suppressive phenotype via LILRB1 . May induce immune activation/suppression via intercellular membrane transfer (trogocytosis), likely enabling interaction with KIR2DL4, which resides mostly in endosomes . Through interaction with the inhibitory receptor CD160 on endothelial cells may control angiogenesis in immune privileged sites . ECO:0000269|PubMed:16366734, ECO:0000269|PubMed:16809620, ECO:0000269|PubMed:19304799, ECO:0000269|PubMed:20179272, ECO:0000269|PubMed:20448110, ECO:0000269|PubMed:23184984, ECO:0000269|PubMed:24453251, ECO:0000269|PubMed:26460007, ECO:0000269|PubMed:27859042, ECO:0000269|PubMed:29262349, [Isoform 3]: Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity . [Isoform 5]: Non-classical major histocompatibility class Ib molecule involved in immune regulatory processes at the maternal-fetal interface . In complex with B2M/beta-2 microglobulin binds a limited repertoire of nonamer self-peptides derived from intracellular proteins including histones and ribosomal proteins . 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 (PubMed:23184984, PubMed:29262349, PubMed:16366734, PubMed:19304799, PubMed: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 . Through interaction with KIR2DL4 receptor on decidual macrophages induces proinflammatory cytokine production mainly associated with tissue remodeling . 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 . Reprograms B cells toward an immune suppressive phenotype via LILRB1 . ECO:0000269|PubMed:20448110, ECO:0000269|PubMed:23184984, ECO:0000269|PubMed:24453251, ECO:0000269|PubMed:29262349, [Isoform 7]: Likely does not bind B2M and presents peptides.

Synonyms:  HLA-G,  HLA-G3,  P17693,  Q29897,  Q31611 ...

Linkouts:  STRING  Pharos  UniProt