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    Keywords: CANCER ; CELLS ; EXPRESSION ; proliferation ; BLOOD ; carcinoma ; CELL ; Germany ; DISEASE ; TISSUE ; MICE ; ANTIGEN ; AUTOIMMUNE-DISEASE ; T-CELL ; T-CELLS ; bone marrow ; BONE-MARROW ; cytokines ; IN-SITU ; CANCER-PATIENTS ; CARCINOMAS ; INVOLVEMENT ; INTERFERON ; FLOW-CYTOMETRY ; pancreatic carcinoma ; chronic pancreatitis ; inflammation ; CYTOKINE ; PANCREATIC-CANCER ; PHASE ; regulatory T cells ; LYMPHOCYTE SUBSETS ; SCLEROSING PANCREATITIS
    Abstract: BACKGROUND & AIMS: Chronic pancreatitis is characterized by alternating phases of acute inflammation and quiescent disease. Involvement of T-cell responses has been suggested, but pancreatitis-specific T cells have not been described. METHODS: We characterized T-cell responses against pancreatitis, pancreatic carcinoma-associated antigens, and tetanus toxoid in the bone marrow, blood, and/or pancreatitis lesions of patients with pancreatitis, pancreatic cancer, and healthy individuals. T cells were functionally characterized by antigen-dependent secretion of interferon (IFN)-gamma, interleukin (Il)-4, and IL-10, which indicate type 1, type 2, or regulatory T-cell responses, respectively. Regulatory T cells were characterized by multicolor flow cytometry. Isolated regulatory T cells were tested for their capacity to recognize pancreatitis-associated antigens and to suppress conventional T cells in an antigen-dependent manner. T cell-derived cytokines in tissue lesions were quantified by enzyme-linked immunosorbent assay. RESULTS: Chronic pancreatitis patients showed similar to pancreatic cancer patients and healthy individuals type 1 T-cell responses against tetanus toxoid; however, they exhibited strong IL-10-based T-cell responses against pancreatitis-associated but not pancreatic carcinoma-associated antigens. T cells from pancreatic cancer patients responded to pancreatic cancer-associated but not pancreatitis-associated antigens with IFN-gamma secretion. Pancreatitis-specific IL-10 responses were mediated by IL-10(+)IFN-gamma(-)FoxP3(+) regulatory T cells, which were expanded in the blood, bone marrow, and pancreatitis lesions and possessed the potential to suppress the proliferation of autologous conventional T cells in an antigen-specific manner. Pancreatitis lesions, in comparison with pancreatic carcinomas, contained increased concentrations of IL-10 and reduced levels of IFN-gamma, suggesting pancreatitis-specific activity of regulatory T cells in situ. CONCLUSIONS: Chronic pancreatitis is associated with disease-specific regulatory T-cell responses
    Type of Publication: Journal article published
    PubMed ID: 19931255
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