Anti-HLA-G Purified Azide Free Monoclonal Antibody

Human leukocyte antigen G (HLA-G), belonging to MHC class I glycoproteins, plays important roles in both physiological and pathological immunotolerance. It gives an inhibitory signal to cytotoxic T cells, NK cells, monocytes, and some other immune cells. It also induces regulatory T cells and anti-inflammatory macrophages. HLA-G is important e.g. for maternal tolerance to the fetus, and for immunomodulation in particular adult tissues, such as in cornea, pancreatic islets, thymus and other. On the other hand, it is expressed in many solid and hematologic malignancies, where it contributes to evasion of the immune surveillance. HLA-G expression pattern in cancer is an important prognostic factor regarding a poor clinical outcome. Unlike most other MHC glycoproteins, HLA-G acts as an immune checkpoint molecule rather than as an antigen presenting molecule. It concerns both transmembrane and soluble HLA-G isoforms. Among other, HLA-G can promote Th2 immunological response and downregulate Th1 immunological response. For its benefits regarding allograft tolerance, including embryo implantation, soluble HLA-G (sHLA-G) can be used as a marker of developmental potential of embryos during the process of in vitro fertilization. Similarly, sHLA-G concentrations in maternal serum are decreased in preeclampsia. Transplanted patients with increased sHLA-G serum levels have improved allograft acceptance. On the other hand, increased sHLA-G can also indicate presence of malignant (sometimes also of benign) tumor cells. Another important topic is induction of HLA-G expression (sometimes associated with shedding of HLA-G from the cell surface) by some anti-cancer or anti-viral therapies, which can weaken the therapy effect. Monitoring of HLA-G in patients thus has a wide usage.

HLA class I histocompatibility antigen, alpha chain G; HLA G antigen; MHC class I antigen G; Soluble HLA class I histocompatibility antigen, alpha chain G; sHLA-G

Recombinant human HLA-G refolded with beta2-microglobulin and peptide. The antibody MEM-G/9 reacts with an extracellular epitope on native form of human HLA-G1 on the cell surface as well as with soluble HLA-G5 isoform in its beta2-microglobulin associated form. Reactivity with HLA-G3 was also reported. The antibody MEM-G/9 is standard reagent thoroughly validated during 3rd International Conference on HLA-G (Paris, 2003) .

Expressed in extravillous trophoblasts and cytotrophoblasts (PubMed:26460007, PubMed:16210391, PubMed:7589701) . Expressed in adult eye (PubMed:1570318) . Expressed in immune cell subsets including monocytes, myeloid and plasmacytoid dendritic cells and regulatory T cells (Tr1) (at protein level) (PubMed:20448110) . Secreted by follicular dendritic cell and follicular helper T cells (PubMed:24453251) . Isoform 5: Detected in physiological fluids including amniotic fluid and serum (PubMed:11137219) . Isoform 7: Expressed in placenta, amniotic membrane, skin cord blood and peripheral blood mononuclear cells (PubMed:11137219) .

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) .