HLA-G Antibody - #DF8559

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. 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.

Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity.

Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity.

Likely does not bind B2M and presents peptides. Negatively regulates NK cell- and CD8+ T cell-mediated cytotoxicity.

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. 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.

Likely does not bind B2M and presents peptides.

Likely does not bind B2M and presents peptides.

N-glycosylated.

Produced by proteolytic cleavage at the cell surface (shedding) by matrix metalloproteinase MMP2.

Cell membrane>Single-pass type I membrane protein. Endoplasmic reticulum membrane. Early endosome membrane.

Secreted.

Cell membrane>Single-pass type I membrane protein.

Cell membrane>Single-pass type I membrane protein.

Cell membrane>Single-pass type I membrane protein.

Secreted. Early endosome.

Secreted.

Secreted.

Cell projection>Filopodium membrane.
Note: HLA-G trogocytosis from extravillous trophoblast's filopodia occurs in the majority of decidual NK cells.

Expressed in adult eye. Expressed in immune cell subsets including monocytes, myeloid and plasmacytoid dendritic cells and regulatory T cells (Tr1)(at protein level). Secreted by follicular dendritic cell and follicular helper T cells. Isoform 5: Detected in physiological fluids including amniotic fluid and serum. Isoform 7: Expressed in placenta, amniotic membrane, skin cord blood and peripheral blood mononuclear cells.

Forms a heterotrimer with B2M and a self-peptide (peptide-bound HLA-G-B2M). HLA-G-B2M complex interacts with components of the antigen processing machinery TAPBP and TAP1-TAP2 complex; this interaction is required for loading of high affinity peptides and heterotrimer translocation to the cell surface. Interacts with CALCR; this interaction is required for appropriate folding. Interacts with COPB1; this interaction mediates the endoplasmic reticulum (ER) retrieval of HLA-G-B2M complexes that bind low affinity peptides. On the cell surface, peptide-bound HLA-G-B2M molecules (referred to as monomers) can form disulfide-linked homomultimers, homodimers and homotrimers. Interacts with KIR2DL4; this interaction is direct. Interacts with LILRB1 and LILRB2 receptors; this interaction is direct. Interacts with CD160; this interactions is direct. Interacts with CD8A homodimer; this interaction is direct and might down-regulate T cell receptor signaling. Isoform 2: Forms a non-disulfide-linked homodimer and interacts with LILRB2.

Belongs to the MHC class I family.