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Diffuse biliary tract involvement mimicking primary sclerosing cholangitis in an experimental model of chronic graft‐versus‐host disease in mice
Author(s) -
OMURA AKITAKA,
KONO NAOKO,
MINATO HIROSHI,
NAKANUMA YASUNI
Publication year - 1998
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/j.1440-1827.1998.tb03927.x
Subject(s) - pathology , bile duct , infiltration (hvac) , transplantation , intrahepatic bile ducts , minor histocompatibility antigen , medicine , fibrosis , primary sclerosing cholangitis , biliary tract , histocompatibility , major histocompatibility complex , biology , immune system , gastroenterology , disease , antigen , immunology , human leukocyte antigen , physics , thermodynamics
Experimental graft‐versushost disease (GVHD) across minor histocompatibility antigens was developed by injecting spleen and bone marrow cells (9:1) of congenic B10.D2 mice into sublethally Irradiated BALB/c mice, and the histologic features of the Iiver were studied for up to 14 months after transplantation. Both intrahepatic and extrahepatic bile ducts were severely involved in the GVHD process and showed features of non‐suppurative cholangitis. Inflammatory cells, mainly lymphocytes, abutted the bile ducts and Infiltrated Into the duct eplthellal layer together with a variety of degenerative changes in the epithelial cells. The peak Inflammatory activity occurred about 2–3 weeks after transplantation. Thereafter, the inflammatory cell Infiltration around the bile ducts and In the bile duct epithelial layer gradually became reduced in severity, although the infiltration persisted during the entire 14 month observation period. Periductal and duct wall fibroplasia began about 1 week after transplantation and gradually progressed. After 2–3 months post‐transplantation, distinct ductal and periductal fibrosis of both intrahepatic and extrahepatic blle ducts was observed. This histologic feature resembled that of primary sclerosing cholangitis (PSC). These results suggest that PSC lesions might develop as a result of chronic cellular Immunologic mechanisms In GVHD across minor histocompatibility barriers.