| Literature DB >> 33435354 |
Laura Elisa Buitrago-Molina1,2, Janine Dywicki1, Fatih Noyan1, Martin Trippler2, Julia Pietrek2, Jerome Schlue3, Michael P Manns1, Heiner Wedemeyer1,2, Elmar Jaeckel1, Matthias Hardtke-Wolenski1,2.
Abstract
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.Entities:
Keywords: IL-17; adenovirus; apoptosis; autoimmune hepatitis; caspase-3; experimental murine hepatitis; formiminotransferase cyclodeaminase; inflammation; liver; spleen
Year: 2021 PMID: 33435354 PMCID: PMC7827897 DOI: 10.3390/biomedicines9010058
Source DB: PubMed Journal: Biomedicines ISSN: 2227-9059