Human leukocyte antigen G,HLA-G ELI

[Isoform 1]: Non-classical major histocompatibility class Ib molecule involved in immune regulatory processes at the maternal-fetal interface (PubMed:23184984, PubMed:29262349, PubMed: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 (PubMed:7584149, PubMed: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 (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 (PubMed:23184984, PubMed:29262349, PubMed:16366734, PubMed:19304799).

Through interaction with KIR2DL4 receptor on decidual macrophages induces proinflammatory cytokine production mainly associated with tissue remodeling (PubMed: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 (PubMed:20448110, PubMed: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 (PubMed:10190900, PubMed:11290782, PubMed:24453251).

Reprograms B cells toward an immune suppressive phenotype via LILRB1 (PubMed:24453251).

May induce immune activation/suppression via intercellular membrane transfer (trogocytosis), likely enabling interaction with KIR2DL4, which resides mostly in endosomes (PubMed:20179272, PubMed:26460007).

Through interaction with the inhibitory receptor CD160 on endothelial cells may control angiogenesis in immune privileged sites (PubMed:16809620).

{ECO:0000269|PubMed:10190900, ECO:0000269|PubMed:11290782, 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, ECO:0000269|PubMed:7584149, ECO:0000269|PubMed:8805247}.; [Isoform 2]: Likely does not bind B2M and presents peptides.

Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed:11290782).

{ECO:0000269|PubMed:11290782, ECO:0000305}.; [Isoform 3]: Likely does not bind B2M and presents peptides.

Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed:11290782).

{ECO:0000269|PubMed:11290782, ECO:0000305}.; [Isoform 4]: Likely does not bind B2M and presents peptides.

Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity (PubMed:11290782).

{ECO:0000269|PubMed:11290782, ECO:0000305}.; [Isoform 5]: Non-classical major histocompatibility class Ib molecule involved in immune regulatory processes at the maternal-fetal interface (PubMed:23184984, PubMed:29262349, PubMed: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 (PubMed:7584149, PubMed: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 (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 (PubMed:23184984, PubMed:29262349, PubMed:16366734, PubMed:19304799).

Through interaction with KIR2DL4 receptor on decidual macrophages induces proinflammatory cytokine production mainly associated with tissue remodeling (PubMed: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 (PubMed:20448110).

Reprograms B cells toward an immune suppressive phenotype via LILRB1 (PubMed:24453251).

{ECO:0000269|PubMed:16366734, ECO:0000269|PubMed:19304799, ECO:0000269|PubMed:20448110, ECO:0000269|PubMed:23184984, ECO:0000269|PubMed:24453251, ECO:0000269|PubMed:29262349, ECO:0000269|PubMed:7584149, ECO:0000269|PubMed:8805247}.; [Isoform 6]: Likely does not bind B2M and presents peptides.

{ECO:0000305}.; [Isoform 7]: Likely does not bind B2M and presents peptides.

{ECO:0000305}.