| Autor: |
Buitrago-Molina LE; Department of Gastroenterology, Hepatology & Endocrinology, Hannover Medical School, D-30625 Hannover, Germany.; Department of Gastroenterology and Hepatology, University Hospital Essen, University Duisburg-Essen, D-45147 Essen, Germany., Dywicki J; Department of Gastroenterology, Hepatology & Endocrinology, Hannover Medical School, D-30625 Hannover, Germany., Noyan F; Department of Gastroenterology, Hepatology & Endocrinology, Hannover Medical School, D-30625 Hannover, Germany., Trippler M; Department of Gastroenterology and Hepatology, University Hospital Essen, University Duisburg-Essen, D-45147 Essen, Germany., Pietrek J; Department of Gastroenterology and Hepatology, University Hospital Essen, University Duisburg-Essen, D-45147 Essen, Germany., Schlue J; Institute of Pathology, Hannover Medical School, D-30625 Hannover, Germany., Manns MP; Department of Gastroenterology, Hepatology & Endocrinology, Hannover Medical School, D-30625 Hannover, Germany., Wedemeyer H; Department of Gastroenterology, Hepatology & Endocrinology, Hannover Medical School, D-30625 Hannover, Germany.; Department of Gastroenterology and Hepatology, University Hospital Essen, University Duisburg-Essen, D-45147 Essen, Germany., Jaeckel E; Department of Gastroenterology, Hepatology & Endocrinology, Hannover Medical School, D-30625 Hannover, Germany., Hardtke-Wolenski M; Department of Gastroenterology, Hepatology & Endocrinology, Hannover Medical School, D-30625 Hannover, Germany.; Department of Gastroenterology and Hepatology, University Hospital Essen, University Duisburg-Essen, D-45147 Essen, Germany. |
| Abstrakt: |
Autoimmune hepatitis (AIH) is detected at a late stage in the course of the disease. Therefore, induction and etiology are largely unclear. It is controversial if the induction of autoimmunity occurs in the liver or in the spleen. In our experimental murine AIH model, the induction of autoimmunity did not occur in the spleen. Instead, a protective role of the spleen could be more likely. Therefore, we splenectomized mice followed by induction of experimental murine AIH. Splenectomized mice presented more severe portal inflammation. Furthermore, these mice had more IL-17, IL-23 receptor (IL-23R) and caspase 3 (casp3) and a decreased amount of erythropoietin in serum, while intrahepatic T cell compartments were unaffected. These results indicate that the spleen is not necessary for induction of AIH, and splenectomy disrupts the ability to immune regulate the intensity of hepatic inflammation, production of IL-17 and apoptosis. |
