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  • 1
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  60. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit den Benelux-Ländern und Bulgarien; 20090524-20090527; Münster; DOCMI.05-04 /20090520/
    Publication Date: 2009-06-30
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 2
    Keywords: brain ; CANCER ; CELLS ; ENDOTHELIAL-CELLS ; EXPRESSION ; tumor ; CELL ; Germany ; LUNG-CANCER ; SYSTEM ; DISEASE ; PROTEIN ; TISSUE ; MICE ; PATIENT ; ANTIGEN ; T-CELL ; T-CELLS ; BONE-MARROW ; MEMORY ; RECOGNITION ; MOUSE ; IDENTIFICATION ; LYMPHOMA ; EFFICACY ; MELANOMA ; MASS-SPECTROMETRY ; HEAD ; NECK ; EPITOPE ; IMMUNOTHERAPY ; IMMUNOGENICITY ; CANCER PATIENTS ; CALCIUM-BINDING PROTEINS ; TUMOR-ASSOCIATED ANTIGENS ; NECK-CANCER ; brain tumor ; head and neck cancer ; endothelial cells ; proteome ; EGFR ; SEPARATION ; EXPRESSION PROFILES ; Type ; HEAD-AND-NECK
    Abstract: Identifying the antigens that have the potential to trigger endogenous antitumor responses in an individual cancer patient is likely to enhance the efficacy of cancer immunotherapy, but current methodologies do not efficiently identify such antigens. This study describes what we believe to be a new method of comprehensively identifying candidate tissue antigens that spontaneously cause T cell responses in disease situations. We used the newly developed automated, two-dimensional chromatography system PF2D to fractionate the proteome of human tumor tissues and tested protein fractions for recognition by preexisting tumor-specific CD4(+) Th cells and CTLs. Applying this method using mice transgenic for a TCR that recognizes an OVA peptide presented by MHC class I, we demonstrated efficient separation, processing, and cross-presentation to CD8(+) T cells by DCs of OVA expressed by the OVA-transfected mouse lymphoma RMA-OVA. Applying this method to human tumor tissues, we identified MUC1 and EGFR as tumor-associated antigens selectively recognized by T cells in patients with head and neck cancer. Finally, in an exemplary patient with a malignant brain tumor, we detected CD4(+) and CD8(+) T cell responses against two novel antigens, transthyretin and calgranulin B/S100A9, which were expressed in tumor and endothelial cells. The immunogenicity of these antigens was confirmed in 4 of 10 other brain tumor patients. This fast and inexpensive method therefore appears suitable for identifying candidate T cell antigens in various disease situations, such as autoimmune and malignant diseases, without being restricted to expression by a certain cell type or HLA allele
    Type of Publication: Journal article published
    PubMed ID: 20458140
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  • 3
    Keywords: RECEPTOR ; CELLS ; proliferation ; CELL ; Germany ; SYSTEM ; DIFFERENTIATION ; MICE ; ACTIVATION ; CUTTING EDGE ; INFECTION ; MECHANISM ; ANTIGEN ; mechanisms ; T-CELL ; T-CELLS ; MEMORY ; NUMBER ; LYMPHOCYTES ; NAIVE ; INTERFERON-GAMMA ; EFFECTOR ; signaling ; EFFECTOR FUNCTION ; HOMEOSTATIC PROLIFERATION ; immunology ; HOMEOSTASIS ; EXPANSION ; SUPPRESSOR-CELLS ; IMMUNE
    Abstract: IFN-gamma regulates multiple processes in the immune system. Although its antimicrobial effector functions are well described, less is known about the mechanisms by which IFN-gamma regulates CD8(+) T cell homeostasis. With the help of adoptive T cell transfers, we show in this study that IEFN-gamma R signaling in CD8(+) T cells is dispensable for expansion, contraction, and memory differentiation in response to peptide vaccination. In contrast, host IFN-gamma R signaling counterregulates CD8(+) T cell responses and the generation of effector memory T cell processes, which are partially regulated by CD11b(+) cells. Similar to vaccination-induced proliferation, host IFN-gamma R signaling limits the expansion of naive CD8(+) T cells and their differentiation into effector memory-like T cells in lymphopenic mice. In contrast to peptide vaccination, IFN-gamma R signaling in CD8(+) T cells contributes to memory fate decision in response to lymphopenia, an effect that is fully reversed by high-affinity TCR ligands. In conclusion, we show that host IFN-gamma R signaling controls the magnitude of CD8(+) T cell responses and subsequent memory differentiation under lymphopenic and nonlymphopenic conditions. In contrast, IFN-gamma R signaling in CD8(+) T cells does not affect cell numbers under either condition, but it directs memory fate decision in response to weak TCR ligands. The Journal of Immunology, 2010, 184: 2855-2862
    Type of Publication: Journal article published
    PubMed ID: 20164422
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