We are analyzing https://link.springer.com/article/10.1007/s00262-008-0587-1.

Title:
HER-2/neu mediated down-regulation of MHC class I antigen processing prevents CTL-mediated tumor recognition upon DNA vaccination in HLA-A2 transgenic mice | Cancer Immunology, Immunotherapy
Description:
To study DNA vaccination directed against human HER-2 in the HHD mouse Tg strain, we created a novel HER-2-expressing syngeneic tumor transplantation model. We found that a DNA vaccine encoding the full length HER-2 DNA protected HHD mice from HER-2+ tumor challenge by a CTL independent mechanism. A more efficient approach to induce HLA-A2 restricted CTLs, through immunization with a multi-epitope DNA vaccine expressing the HLA-A2 restricted HER-2 369–377, 435–443 and 689–697 epitopes, resulted in high numbers of peptide specific T cells but failed to induce tumor protection. Subsequently we discovered that HER-2 transfected tumor cells down-regulated MHC class I antigen expression and exhibited a series of defects in the antigen processing pathway which impaired the capacity to produce and display MHC class I peptide-ligands to specific CTLs. Our data demonstrate that HER-2 transfection is associated with defects in the MHC class I presentation pathway, which may be the underlying mechanism behind the inability of CTLs to recognize tumors in this HLA-A2 transgenic model. As defective MHC class I presentation may be a common characteristic of HER-2 expressing tumors, vaccines targeting HER-2 should aim at inducing an integrated immune response where also CD4+ T cells and antibodies are important components.
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Keywords {🔍}

article, cancer, google, scholar, herneu, dna, class, tumor, cells, mhc, transgenic, mice, kiessling, vaccine, human, immunol, res, antigen, processing, vaccination, seliger, peptide, tumors, cytotoxic, int, hlaa, vertuani, vaccines, privacy, cookies, content, ctl, immunization, specific, access, cell, lymphocytes, data, protection, information, publish, search, immunotherapy, simona, triulzi, roos, charo, lemonnier, induce, ctls,

Topics {✒️}

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Schema {🗺️}

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         headline:HER-2/neu mediated down-regulation of MHC class I antigen processing prevents CTL-mediated tumor recognition upon DNA vaccination in HLA-A2 transgenic mice
         description:To study DNA vaccination directed against human HER-2 in the HHD mouse Tg strain, we created a novel HER-2-expressing syngeneic tumor transplantation model. We found that a DNA vaccine encoding the full length HER-2 DNA protected HHD mice from HER-2+ tumor challenge by a CTL independent mechanism. A more efficient approach to induce HLA-A2 restricted CTLs, through immunization with a multi-epitope DNA vaccine expressing the HLA-A2 restricted HER-2 369–377, 435–443 and 689–697 epitopes, resulted in high numbers of peptide specific T cells but failed to induce tumor protection. Subsequently we discovered that HER-2 transfected tumor cells down-regulated MHC class I antigen expression and exhibited a series of defects in the antigen processing pathway which impaired the capacity to produce and display MHC class I peptide-ligands to specific CTLs. Our data demonstrate that HER-2 transfection is associated with defects in the MHC class I presentation pathway, which may be the underlying mechanism behind the inability of CTLs to recognize tumors in this HLA-A2 transgenic model. As defective MHC class I presentation may be a common characteristic of HER-2 expressing tumors, vaccines targeting HER-2 should aim at inducing an integrated immune response where also CD4+ T cells and antibodies are important components.
         datePublished:2008-09-27T00:00:00Z
         dateModified:2008-09-27T00:00:00Z
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            DNA vaccine
            HER-2
            MHC class I
            Antigen processing
            Oncology
            Immunology
            Cancer Research
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      headline:HER-2/neu mediated down-regulation of MHC class I antigen processing prevents CTL-mediated tumor recognition upon DNA vaccination in HLA-A2 transgenic mice
      description:To study DNA vaccination directed against human HER-2 in the HHD mouse Tg strain, we created a novel HER-2-expressing syngeneic tumor transplantation model. We found that a DNA vaccine encoding the full length HER-2 DNA protected HHD mice from HER-2+ tumor challenge by a CTL independent mechanism. A more efficient approach to induce HLA-A2 restricted CTLs, through immunization with a multi-epitope DNA vaccine expressing the HLA-A2 restricted HER-2 369–377, 435–443 and 689–697 epitopes, resulted in high numbers of peptide specific T cells but failed to induce tumor protection. Subsequently we discovered that HER-2 transfected tumor cells down-regulated MHC class I antigen expression and exhibited a series of defects in the antigen processing pathway which impaired the capacity to produce and display MHC class I peptide-ligands to specific CTLs. Our data demonstrate that HER-2 transfection is associated with defects in the MHC class I presentation pathway, which may be the underlying mechanism behind the inability of CTLs to recognize tumors in this HLA-A2 transgenic model. As defective MHC class I presentation may be a common characteristic of HER-2 expressing tumors, vaccines targeting HER-2 should aim at inducing an integrated immune response where also CD4+ T cells and antibodies are important components.
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      dateModified:2008-09-27T00:00:00Z
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         DNA vaccine
         HER-2
         MHC class I
         Antigen processing
         Oncology
         Immunology
         Cancer Research
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      name:Immune and Gene Therapy Unit, Cancer Centrum Karolinska, Karolinska Hospital, Stockholm, Sweden
      name:Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden
      name:Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden
      name:Max-Delbrück-Centrum, Berlin, Germany
      name:Hollings Cancer Center, Medical University of South Carolina, Charleston, USA
      name:Unité d’Immunité Cellulaire Antivirale, Institut Pasteur, Paris, France
      name:Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden
      name:Institute of Medical Immunology, Martin Luther University Halle-Wittenberg, Halle, Germany
      name:Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden
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