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  • INDUCTION  (3)
  • 1
    Keywords: APOPTOSIS ; CELLS ; ENDOTHELIAL-CELLS ; tumor ; TUMOR-CELLS ; CELL ; Germany ; IN-VIVO ; VIVO ; SYSTEM ; liver ; MICE ; MECHANISM ; INDUCTION ; ANTIGEN ; ANTIGENS ; DENDRITIC CELLS ; T cell ; T cells ; T-CELLS ; TOLERANCE ; BONE-MARROW ; CANCER-CELLS ; NATURAL-KILLER-CELLS ; FRAGMENTS ; FAILURE ; ADAPTIVE IMMUNITY ; TUMOR CELLS ; ELIMINATION ; IMMUNE ESCAPE ; IMMUNE-SYSTEM ; ESCAPE ; CYTOKINE PRODUCTION ; TUMOR-CELL ; KUPFFER CELLS ; in vivo ; FRAGMENT ; CD8(+) T cell ; COLON-CARCINOMA CELLS ; liver sinusoidal endothelial cells ; NKT CELLS ; PERFORIN/GRANZYME PATHWAY ; sinusoidal endothelial cells
    Abstract: Development of tumor-specific T cell tolerance contributes to the failure of the immune system to eliminate tumor cells. Here we report that hematogenous dissemination of tumor cells followed by their elimination and local removal of apoptotic tumor cells in the liver leads to subsequent development of T cell tolerance towards antigens associated with apoptotic tumor cells. We provide evidence that liver sinusoidal. endothelial cells (LSEC) remove apoptotic cell fragments generated by induction of tumor cell apoptosis through hepatic NK1.1(+) cells. Antigen associated with apoptotic cell material is processed and cross-presented by LSEC to CD8(+) T cells, leading to induction of CD8(+) T cell tolerance. Adoptive transfer of LSEC isolated from mice challenged previously with tumor cells promotes development of CD8(+) T cell tolerance towards tumor-associated antigen in vivo. Our results indicate that hematogenous dissemination of tumor cells, followed by hepatic tumor cell elimination and local cross-presentation of apoptotic tumor cells by LSEC and subsequent CD8(+) T cell tolerance induction, represents a novel mechanism operative in tumor immune escape
    Type of Publication: Journal article published
    PubMed ID: 17039564
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  • 2
    Keywords: CANCER ; EXPRESSION ; CELL ; Germany ; IN-VIVO ; THERAPY ; VIVO ; SYSTEM ; TOOL ; liver ; GENE ; GENE-EXPRESSION ; GENES ; PROTEIN ; MICE ; MACROPHAGES ; INDUCTION ; tumour ; BIOLOGY ; culture ; MOUSE ; gene expression ; VECTORS ; PROMOTER ; REGION ; VACCINES ; REGIONS ; DELIVERY ; Jun ; CARRIERS ; GREEN FLUORESCENT PROTEIN ; LUCIFERASE ; CYTOSINE DEAMINASE ; RE ; THERAPIES ; REPORTER GENE ; CARRIER ; HISTOLOGY ; in vivo ; E ; TOOLS ; spleen ; microbiology ; ENGLAND ; host ; FLUORESCENT PROTEIN ; FLUORESCENT ; PLASMIDS ; bacterial ; ARABAD PROMOTER ; tumour therapy
    Abstract: We have used Salmonella enterica serovar Typhimurium (S. typhimurium) which are able to colonize tumours besides spleen and liver. Bacteria were equipped with constructs encoding green fluorescent protein or luciferase as reporters under control of the promoter P-BAD that is inducible with L-arabinose. Reporter genes could be induced in culture but also when the bacteria resided within the mouse macrophages J774A.1. More important, strong expression of reporters by the bacteria could be detected in mice after administration of L-arabinose. This was especially pronounced in bacteria colonizing tumours. Histology demonstrated that the bacteria had accumulated in and close to necrotic areas of tumours. Bacterial gene induction was observed in both regions. P-BAD is tightly controlled also in vivo because gene E of bacteriophage Phi X174 could be introduced as inducible suicide gene. The possibility to deliberately induce genes in bacterial carriers within the host should render them extremely powerful tools for tumour therapy
    Type of Publication: Journal article published
    PubMed ID: 17298393
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  • 3
    Keywords: IN-VIVO ; DIFFERENTIATION ; MICE ; ACTIVATION ; IFN-GAMMA ; INDUCTION ; AUTOIMMUNE-DISEASE ; DENDRITIC CELLS ; IL-2 ; inflammation ; AUTOIMMUNITY ; TGF-BETA ; T(H)17 ; TH17 CELLS
    Abstract: T helper 17 (Th17) cell development is driven by cytokines including transforming growth factor-beta (TGF-beta), interleukin-6 (IL-6), IL-1, and IL-23. Regulatory T (Treg) cells can provide the TGF-beta in vitro, but their role in vivo remains unclear, particularly because Treg Th17 cell-associated autoimmunity. We used mice expressing Diphtheria toxin receptor under control of the Foxp3 promoter to deplete Foxp3(+) Treg cells in adult mice during in vivo Th17 cell priming. Treg cell depletion resulted in a reduced frequency of antigen-specific IL-17 producers in draining lymph nodes and blood, correlating with reduced inflammatory skin responses. In contrast, Treg cells did not promote IL-17 secretion after initial activation stages. Treg cell production of TGF-beta was not required for Th17 cell promotion, and neither was suppression of Th1 cell-associated cytokines. Rather, regulation of IL-2 availability and resultant signaling through CD25 by Treg cells was found to play an important role
    Type of Publication: Journal article published
    PubMed ID: 21435588
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