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  • Functional expression and release of ligands for the activating immunoreceptor NKG2D in leukemia 12714493

    NKG2D ligands (NKG2DLs) mark malignant cells for recognition by natural killer (NK) cells and cytotoxic T lymphocytes via the activating immunoreceptor NKG2D. This led to the hypothesis that NKG2DLs play a critical role in tumor immune surveillance. The human NKG2DLs MICA and MICB are expressed on tumors of epithelial origin in vivo. For the other recently described set of human NKG2DLs, the UL16-binding proteins (ULBPs), expression in vivo is as yet undefined. In this study we investigated expression and function of NKG2DLs in leukemia using a panel of newly generated NKG2DL-specific monoclonal antibodies. We report that leukemia cells from patients variously express MIC and ULBP molecules on the cell surface with MICA most frequently detected. Patient leukemia cells expressing MICA were lysed by NK cells in an NKG2D-dependent fashion. Sera of patients, but not of healthy donors, contained elevated levels of soluble MICA (sMICA). We also detected increased sMICB levels in patient sera using a newly established MICB-specific enzyme-linked immunosorbent assay. Reduction of leukemia MIC surface expression by shedding may impair NKG2D-mediated immune surveillance of leukemias. In addition, determination of sMICA and sMICB levels may be implemented as a prognostic parameter in patients with hematopoietic malignancies.
    Dokumententyp:
    Referenz
    Produkbestellnummer:
    Mehrere
    Produktbezeichnung:
    Mehrere

  • Selective intracellular retention of virally induced NKG2D ligands by the human cytomegalovirus UL16 glycoprotein 12594848

    Human cytomegalovirus (HCMV) has evolved a multitude of molecular mechanisms to evade the antiviral immune defense of the host. Recently, using soluble recombinant molecules, the HCMV UL16 glycoprotein was shown to interact with some ligands of the activating immunoreceptor NKG2D and, therefore, may also function as a viral immunomodulator. However, the role of UL16 during the course of HCMV infection remained unclear. Here, we demonstrate that HCMV infection of fibroblasts induces expression of all known NKG2D ligands (NKG2DL). However, solely MICA and ULBP3 reach the cellular surface to engage NKG2D, whereas MICB, ULBP1 and ULBP2 are selectively retained in the endoplasmic reticulum by UL16. UL16-mediated reduction of NKG2DL cell surface density diminished NK cytotoxicity. Thus, UL16 functions by capturing activating ligands for cytotoxic lymphocytes that are synthesized in response to HCMV infection.
    Dokumententyp:
    Referenz
    Produkbestellnummer:
    Mehrere
    Produktbezeichnung:
    Mehrere

  • Anti-MICA, clone AMO-1 - Q3490935

    Dokumententyp:
    Analysenzertifikat
    Chargennummer:
    Q3490935
    Produkbestellnummer:
    MABF2220-100UG
    Produktbezeichnung:
    Anti-MICA Antibody, clone AMO-1

  • Anti-MICA, clone AMO-1 - 3911794

    Dokumententyp:
    Analysenzertifikat
    Chargennummer:
    3911794
    Produkbestellnummer:
    MABF2220-100UG
    Produktbezeichnung:
    Anti-MICA Antibody, clone AMO-1

  • Anti-MICA, clone AMO-1 - 4010120

    Dokumententyp:
    Analysenzertifikat
    Chargennummer:
    4010120
    Produkbestellnummer:
    MABF2220-100UG
    Produktbezeichnung:
    Anti-MICA Antibody, clone AMO-1

  • Anti-MICA, clone AMO-1 - 3992937

    Dokumententyp:
    Analysenzertifikat
    Chargennummer:
    3992937
    Produkbestellnummer:
    MABF2220-100UG
    Produktbezeichnung:
    Anti-MICA Antibody, clone AMO-1

  • Anti-MICA, clone AMO-1 - 4113035

    Dokumententyp:
    Analysenzertifikat
    Chargennummer:
    4113035
    Produkbestellnummer:
    MABF2220-100UG
    Produktbezeichnung:
    Anti-MICA Antibody, clone AMO-1