This antibody recognizes native surface-expressed HLA-E, but not denaturated heavy chain of HLA-E. HLA-E belongs to the MHC Class I molecules (MHC Class Ib; nonclassical) and it is expressed on many types of the human cells.

Applications

Flow Cytometry, IP, IHC-P

Recommander des dilutions

IHC-P: 10 µg/ml; Positive Control: spleen, Flow Cytometry: 1-4 µg/ml.

Reactivité

Human

Immunogène

Bacterially expressed recombinant HLA-E refolded with beta 2-Microglobulin and peptide.

Hôte

Mouse

Clonalité

Monoclonal

Clone

MEM-E/07

Isotype

IgG1

Conjuguer

Unconjugated

Purification

Protein A chromatography.

Concentration

1 mg/ml

Forme du produit

Liquid

Formulation

Supplied in Phosphate Buffered Saline, pH 7.4, with 15 mM Sodium Azide.

Stockage

Shipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze/thaw cycles.

Synonymes

EA1.2, EA2.1, HLA 6.2, HLA class I histocompatibility antigen alpha chain E, HLA class I histocompatibility antigen E alpha chain, HLA class I histocompatibility antigen E alpha chain precursor, HLA6.2, HLAE, Lymphocyte antigen, Major histocompatibility complex class I E, MHC, MHC class I antigen E, MHC HLA E alpha 1, MHC HLA E alpha 2.1, QA1

Contrôles isotype

Anticorps secondaires appropriés

Avertissement

Ce produit est uniquement destiné à la recherche. Il n'est pas destiné à un usage diagnostique ou thérapeutique.

Images (1)

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Figure 1: Immunohistochemistry - Anti-HLA E Antibody [MEM-E/07] (A86034)

Immunohistochemistry staining of human spleen (paraffin sections) with Anti-HLA E Antibody (A86034).

Références pour cet ID de clone (6)

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The HCMV membrane glycoprotein US10 selectively targets HLA-G for degradation.

Références : Anti-HLA E Antibody [MEM-E/07] (ab11820)

Résumé :

Human cytomegalovirus (HCMV) encodes an endoplasmic reticulum (ER)-resident transmembrane glycoprotein, US10, expressed early in the replicative cycle of HCMV as part of the same cluster that encodes the known immunoevasins US2, US3, US6, and US11. We show that US10 down-regulates cell surface expression of HLA-G, but not that of classical class I MHC molecules. The unique and short cytoplasmic tail of HLA-G (RKKSSD) is essential in its role as a US10 substrate, and a tri-leucine motif in the cytoplasmic tail of US10 is responsible for down-regulation of HLA-G. Both the kinetics of HLA-G degradation and the mechanisms responsible appear to be distinct from those used by the US2 and US11 pathways, suggesting the existence of a third route of protein dislocation from the ER. We show that US10-mediated degradation of HLA-G interferes with HLA-G-mediated NK cell inhibition. Given the role of HLA-G in protecting the fetus from attack by the maternal immune system and in directing the differentiation of human dendritic cells to promote the evolution of regulatory T cells, HCMV likely targets the HLA-G-dependent axis of immune recognition no less efficiently than it interferes with classical class I MHC-restricted antigen presentation.

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Inhibition of ERK and proliferation in NK cell lines by soluble HLA-E released from Japanese encephalitis virus infected cells.

Références : Anti-HLA E Antibody [MEM-E/07] (ab11820)

Résumé :

Productive infection of human endothelial cells with Japanese encephalitis virus (JEV), a single stranded RNA virus induces shedding of sHLA-E. We show here that sHLA-E that is released upon infection with this flavivirus can inhibit IL-2 and PMA mediated ERK 1/2 phosphorylation in two NK cell lines, Nishi and NKL. Virus infected or IFN-? treated cell culture supernatants containing sHLA-E were found to partially inhibit IL-2 mediated induction of CD25 molecules on NKL cells. It was also found that sHLA-E could inhibit IL-2 induced [(3)H]-thymidine incorporation suggesting that, similar to cell surface expressed HLA-E, sHLA-E could also inhibit NK cell responses. Hence JEV-induced shedding of sHLA-E needs further investigation to better understand immune responses in JEV infections since it may have a role in viral evasion of NK cell responses.

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Infection of human endothelial cells by Japanese encephalitis virus: increased expression and release of soluble HLA-E.

Références : Anti-HLA E Antibody [MEM-E/07] (ab11820)

Résumé :

Japanese encephalitis virus (JEV) is a single stranded RNA virus that infects the central nervous system leading to acute encephalitis in children. Alterations in brain endothelial cells have been shown to precede the entry of this flavivirus into the brain, but infection of endothelial cells by JEV and their consequences are still unclear. Productive JEV infection was established in human endothelial cells leading to IFN-ß and TNF-a production. The MHC genes for HLA-A, -B, -C and HLA-E antigens were upregulated in human brain microvascular endothelial cells, the endothelial-like cell line, ECV 304 and human foreskin fibroblasts upon JEV infection. We also report the release/shedding of soluble HLA-E (sHLA-E) from JEV infected human endothelial cells for the first time. This shedding of sHLA-E was blocked by an inhibitor of matrix metalloproteinases (MMP). In addition, MMP-9, a known mediator of HLA solubilisation was upregulated by JEV. In contrast, human fibroblasts showed only upregulation of cell-surface HLA-E. Addition of UV inactivated JEV-infected cell culture supernatants stimulated shedding of sHLA-E from uninfected ECV cells indicating a role for soluble factors/cytokines in the shedding process. Antibody mediated neutralization of TNF-a as well as IFNAR receptor together not only resulted in inhibition of sHLA-E shedding from uninfected cells, it also inhibited HLA-E and MMP-9 gene expression in JEV-infected cells. Shedding of sHLA-E was also observed with purified TNF-a and IFN-ß as well as the dsRNA analog, poly (I:C). Both IFN-ß and TNF-a further potentiated the shedding when added together. The role of soluble MHC antigens in JEV infection is hitherto unknown and therefore needs further investigation.

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Epstein-Barr virus peptide presented by HLA-E is predominantly recognized by CD8(bright) cells in multiple sclerosis patients.

Références : Anti-HLA E Antibody [MEM-E/07] (ab11820)

Résumé :

Multiple sclerosis (MS) is associated with Epstein-Barr virus (EBV) infection, but impaired immune suppression may be part of the disease pathogenesis. CD8(+) T cells that are restricted by HLA-E exert an important immunoregulatory mechanism. To explore how EBV might interfere with immune regulation, we examined the expression of HLA-E and the frequency of CD8(+) cells recognizing HLA-E, presenting either an EBV peptide from the BZLF1 protein or a signal sequence peptide from HLA-A2, in relapsing remitting (MS-RR), primary progressive (MS-PP) MS patients, and healthy controls (HC). Treatment with IFN-a or EBV increased HLA-E expression on CD4(+) cells. However, only MS-PP had increased expression of HLA-E on resting CD4(+) cells when compared with HC (p<0.005). CD8(+) cells were divided into CD8(bright) and CD8(dim) cells by flow cytometry analyses. MS-RR had significantly fewer CD8(dim) cells than HC (p<0.003). Flow cytometry analyses were performed with HLA-E tetramers folded in the presence of the EBV or HLA-A2 peptide to identify HLA-E-interacting cells. MS-RR had increased frequency of CD8(bright) cells recognizing HLA-E/A2 (p=0.006) and HLA-E/BZLF1 (p=0.016). Conversely, MS-RR had fewer CD8(dim) cells that recognized HLA-E/BZLF1 (p=0.001), but this could be attributed to the overall lower number of CD8(dim) cells in MS-RR. Whereas HLA-E/A2 was predominantly recognized by CD8(dim) cells, HLA-E/BZLF1 was predominantly recognized by CD8(bright) cells in MS-RR and MS-PP, but not in HC. As expected, HLA-E/A2 was also recognized by CD8-negative cells in a CD94-dependent manner, whereas HLA-E/BZLF1 was poorly recognized in all groups by CD8-negative cells. These data demonstrate that MS-RR patients have expanded their CD8(bright) cells recognizing HLA-E/BZLF1. Moreover, HLA-E/BZLF1 appears to be recognized by the immune system in a different manner than HLA-E/A2.

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Unravelling the T-cell-mediated autoimmune attack on CNS myelin in a new primate EAE model induced with MOG34-56 peptide in incomplete adjuvant.

Références : Anti-HLA E Antibody [MEM-E/07] (ab11820)

Résumé :

Induction of experimental autoimmune encephalomyelitis (EAE) has been documented in common marmosets using peptide 34-56 from human myelin/oligodendrocyte glycoprotein (MOG(34-56) ) in incomplete Freund's adjuvant (IFA). Here, we report that this EAE model is associated with widespread demyelination of grey and white matter. We performed an in-depth analysis of the specificity, MHC restriction and functions of the activated T cells in the model, which likely cause EAE in an autoantibody-independent manner. T-cell lines isolated from blood and lymphoid organs of animals immunized with MOG(34-56) displayed high production of IL-17A and specific lysis of MOG(34-56) -pulsed EBV B-lymphoblastoid cells as typical hallmarks. Cytotoxicity was directed at the epitope MOG(40-48) presented by the non-classical MHC class Ib allele Caja-E, which is orthologue to HLA-E and is expressed in non-inflamed brain. In vivo activated T cells identified by flow cytometry in cultures with MOG(34-56,) comprised CD4(+) CD56(+) and CD4(+) CD8(+) CD56(+) T cells. Furthermore, phenotypical analysis showed that CD4(+) CD8(+) CD56(+) T cells also expressed CD27, but CD16, CD45RO, CD28 and CCR7 were absent. These results show that, in the MOG34-56/IFA marmoset EAE model, a Caja-E-restricted population of autoreactive cytotoxic T cells plays a key role in the process of demyelination in the grey and white matter.

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HLA-E surface expression is independent of the availability of HLA class I signal sequence-derived peptides in human tumor cell lines.

Références : Anti-HLA E Antibody [MEM-E/07] (ab11820)

Résumé :

Human leukocyte antigen (HLA)-E is a nonclassic HLA class I molecule whose expression at the cell surface of tumor cells might allow them to escape T- and natural killer (NK)-cell immune surveillance. In this study, we analyzed HLA-E expression in a panel of human HLA-typed tumor cell lines of different histotypes by flow cytometry with anti-HLA-E monoclonal antibodies and by reverse transcriptase-polymerase chain reaction. Although specific HLA-E transcripts were detected in all cell lines, except in HELA, surface expression was detected at different intensities on seven (23%) of 30 cell lines with higher frequency and intensity among osteosarcoma cell lines. HLA-E-positive tumor cell lines mainly expressed the HLA-A*02 class I allele. Some tumor cell lines demonstrating HLA class I A* or Cw* alleles, which we expected to allow HLA-E surface expression on the basis of reported data on lymphoid cells, instead were HLA-E negative. All tumor cell lines were either tapasin and TAP-1 positive by flow cytometry, except two osteosarcoma cell lines, a finding that suggests an intact assembly machinery for peptide loading. We conclude that the concomitant presence of the appropriate HLA class I alleles with leader sequence-derived peptides and HLA-E heavy chain may not be sufficient to allow HLA-E surface expression in tumor cell lines as opposed to lymphoid cells.

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