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  1. Article: Reconstitution of expression of H-2K region-encoded murine MHC class I glycoproteins in MHC class I-deficient B16BL6 melanoma cells affects the expression and function of antigen-processing machinery.

    Tsory, Sylvia / Kellman-Pressman, Sigal / Fishman, Daniel / Segal, Shraga

    Immunology letters

    2006  Volume 102, Issue 2, Page(s) 237–240

    Abstract: We have recently reported that reconstitution of expression of major histocompatibility complex (MHC) class I glycoproteins in MHC-deficient and highly metastatic B16BL6 melanoma cells attenuates their malignant capacities by modulation of ... ...

    Abstract We have recently reported that reconstitution of expression of major histocompatibility complex (MHC) class I glycoproteins in MHC-deficient and highly metastatic B16BL6 melanoma cells attenuates their malignant capacities by modulation of compartmentalization and functions of cell membrane receptors for growth factors [Assa-Kunik E, et al. J Immunol 2003;171:2945-52]. Our present study provides evidence that re-expression of an H-2K MHC class I-encoding gene in these cells also augments the expression of the Tap-2 peptide transporter and the inducible proteasome subunits, i.e. Lmp-2, Lmp-7 and Lmp-10. Up-regulation of inducible proteasome subunits was also followed by a significant changed in the proteolytic activity of the proteasome complex. We suggest that, in addition to providing a framework for proper presentation of antigenic peptides, MHC class I glycoproteins may regulate the immune response by modulating the expression and function of other genes, whose products are essential for proper antigen processing and presentation.
    MeSH term(s) ATP-Binding Cassette Transporters/metabolism ; ATP-Binding Cassette, Sub-Family B, Member 3 ; Animals ; Antigen Presentation ; Cell Line, Tumor ; Clone Cells ; Genes, MHC Class I ; H-2 Antigens/genetics ; Melanoma, Experimental/genetics ; Mice ; Proteasome Endopeptidase Complex/metabolism ; Up-Regulation
    Chemical Substances ATP-Binding Cassette, Sub-Family B, Member 3 ; H-2 Antigens ; Tap2 protein, mouse ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
    Language English
    Publishing date 2006-02-15
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 445150-8
    ISSN 1879-0542 ; 0165-2478
    ISSN (online) 1879-0542
    ISSN 0165-2478
    DOI 10.1016/j.imlet.2005.08.008
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1512: Show issues Location:
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  2. Article: Attenuation of the Fas-L independent B16BL6 melanoma lymphocidic capacity by H-2K class I molecules.

    Kellman-Pressman, Sigal / Fishman, Daniel / Tsory, Sylvia / Segal, Shraga

    Immunology letters

    2005  Volume 100, Issue 2, Page(s) 146–152

    Abstract: We have previously reported that the capacity of highly malignant B16BL6 murine melanoma cells to induce cell death in naive syngeneic lymphocytes stems from the absence of major histocompatibility complex (MHC) class I glycoproteins in these melanoma ... ...

    Abstract We have previously reported that the capacity of highly malignant B16BL6 murine melanoma cells to induce cell death in naive syngeneic lymphocytes stems from the absence of major histocompatibility complex (MHC) class I glycoproteins in these melanoma cells. Our present study provides evidence that the above-mentioned lymphocidic activities of B16BL6 cells are selectively attenuated when the expression of H-2K (but not H-2D or H-2L) MHC class I glycoproteins is reconstituted in these cells. The induction of apoptosis in naive lymphocytes by H-2K-deficient melanoma cells does not involve the Fas ligand (Fas-L)/FAS signaling module, as demonstrated by employing lymphocytes derived from Fas-L(gld)- or Fas(lpr)-deficient mice in co-culture experiments. Furthermore, these tumor cells fail to induce Fas-L-mediated fratricide in co-cultured lymphocytes and do not express Fas-L either when grown alone or co-cultured with lymphocytes. These findings explain the previously widely reported selective down-regulation of certain MHC class I-encoded glycoproteins (H-2K, bur not H-2D or H-2L) during tumor progression. Namely, the initiation of an effective immune response against H-2K-deficient cells could be abrogated at very early steps, as the result of the induction of Fas-L/Fas-independent cell death among naive lymphoid cells.
    MeSH term(s) Animals ; Apoptosis/immunology ; Coculture Techniques ; Fas Ligand Protein ; H-2 Antigens/genetics ; H-2 Antigens/immunology ; Histocompatibility Antigen H-2D ; Lymphocytes/immunology ; Melanoma, Experimental/immunology ; Melanoma, Experimental/pathology ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/immunology ; Mice ; Mice, Inbred C57BL ; Neoplasm Transplantation ; RNA, Messenger/analysis ; Spleen/cytology ; Spleen/immunology ; Time Factors ; Transfection ; Tumor Cells, Cultured ; Tumor Necrosis Factors/genetics ; Tumor Necrosis Factors/immunology
    Chemical Substances Fas Ligand Protein ; Fasl protein, mouse ; H-2 Antigens ; H-2K(K) antigen ; Histocompatibility Antigen H-2D ; Membrane Glycoproteins ; RNA, Messenger ; Tumor Necrosis Factors
    Language English
    Publishing date 2005-09-15
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 445150-8
    ISSN 1879-0542 ; 0165-2478
    ISSN (online) 1879-0542
    ISSN 0165-2478
    DOI 10.1016/j.imlet.2005.03.016
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  3. Article: Alterations in the expression of MHC class I glycoproteins by B16BL6 melanoma cells modulate insulin receptor-regulated signal transduction and augment [correction of augments] resistance to apoptosis.

    Assa-Kunik, Efrat / Fishman, Daniel / Kellman-Pressman, Sigal / Tsory, Sylvia / Elhyany, Shira / Baharir, Ofer / Segal, Shraga

    Journal of immunology (Baltimore, Md. : 1950)

    2003  Volume 171, Issue 6, Page(s) 2945–2952

    Abstract: In a variety of malignancies, the immune-escape phenotype is associated, in part, with the inability of tumor cells to properly present their Ags to CTLs due to a deranged expression of MHC class I glycoproteins. However, these molecules were found to ... ...

    Abstract In a variety of malignancies, the immune-escape phenotype is associated, in part, with the inability of tumor cells to properly present their Ags to CTLs due to a deranged expression of MHC class I glycoproteins. However, these molecules were found to possess broader nonimmune functions, including participation in signal transduction and regulation of proliferation, differentiation, and sensitivity to apoptosis-inducing factors; processes, which are characteristically impaired during malignant transformation. We investigated whether the deranged expression of MHC class I expression by tumor cells could affect proper receptor-mediated signal transduction and accentuate their malignant phenotype. The malignant and H-2K murine MHC class I-deficient B16BL6 melanoma cells were characterized by an attenuated capacity to bind insulin due to the retention of corresponding receptor in intracellular stores. The restoration of H-2K expression in these cells, which abrogated their capacity to form tumors in mice, enhanced membrane translocation of the receptor, presumably, by modulating its glycosylation. The addition of insulin to H-2K-expressing melanoma cells cultured in serum-free conditions precluded apoptotic death by up-regulating the activity of protein kinase B (PKB)/Akt. In contrast, the deficiency for H-2K characteristic to the malignant clones was associated with a constitutive high activity of PKB/Akt, which rendered them resistant to apoptosis, induced by deprivation of serum-derived growth factors. The possibility to correct the regulation of PKB/Akt activity by restoration of H-2K expression in B16BL6 melanoma cells may be considered as an attractive approach for cancer therapy, since an aberrant activation of this enzyme is characteristic to resistant malignancies.
    MeSH term(s) Adjuvants, Immunologic/biosynthesis ; Adjuvants, Immunologic/genetics ; Adjuvants, Immunologic/metabolism ; Adjuvants, Immunologic/physiology ; Animals ; Apoptosis/immunology ; Cell Line, Tumor ; Clone Cells ; Glycoproteins/biosynthesis ; Glycoproteins/genetics ; Glycoproteins/metabolism ; Glycoproteins/physiology ; Glycosylation ; Growth Substances/deficiency ; H-2 Antigens/biosynthesis ; H-2 Antigens/genetics ; H-2 Antigens/metabolism ; H-2 Antigens/physiology ; Immunity, Innate ; Insulin/metabolism ; Melanoma, Experimental/enzymology ; Melanoma, Experimental/immunology ; Melanoma, Experimental/metabolism ; Mice ; Mice, Inbred C57BL ; Protein Binding/immunology ; Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-akt ; Receptor, Insulin/metabolism ; Receptor, Insulin/physiology ; Signal Transduction/immunology
    Chemical Substances Adjuvants, Immunologic ; Glycoproteins ; Growth Substances ; H-2 Antigens ; Insulin ; Proto-Oncogene Proteins ; Receptor, Insulin (EC 2.7.10.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2003-09-04
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.171.6.2945
    Database MEDical Literature Analysis and Retrieval System OnLINE

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