Pathology and Immunopathology of Primary Biliary Cirrhosis With Emphasis On Bile Duct Lesions: Recent Progress

1995 ◽  
Vol 15 (04) ◽  
pp. 313-328 ◽  
Author(s):  
Yasuni Nakanuma ◽  
Koichi Tsuneyama ◽  
M. Gershwin ◽  
Mitsue Yasoshima
2017 ◽  
pp. 73-84
Author(s):  
Hayato Baba ◽  
Ayumi Sugitani ◽  
Ryusei Takahashi ◽  
Kouki Kai ◽  
Yuki Moritoki ◽  
...  

2013 ◽  
Vol 67 (5) ◽  
pp. 396-402 ◽  
Author(s):  
Kenichi Harada ◽  
Yuko Kakuda ◽  
Yasunori Sato ◽  
Hiroko Ikeda ◽  
Shinji Shimoda ◽  
...  

2000 ◽  
Vol 31 (2) ◽  
pp. 179-184 ◽  
Author(s):  
Mitsuhiro Iwata ◽  
Kenichi Harada ◽  
Naoko Kono ◽  
Shuichi Kaneko ◽  
Kenichi Kobayashi ◽  
...  

2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
Motoko Sasaki ◽  
Yasuni Nakanuma

Primary biliary cirrhosis (PBC) is a chronic cholestatic liver disease characterized serologically by the high prevalence of anti-mitochondrial autoantibodies (AMAs) and histologically by the cholangitis of small bile ducts, eventually followed by extensive loss of the small bile duct. An autoimmune pathogenesis is suggested by clinical and experimental studies, but there remain issues regarding the etiology, the significance of AMAs in the pathogenesis of bile duct lesions, and so on. The unique properties of apoptosis in biliary epithelial cells (BECs), in which there is exposure of autoantigen to the effectors of the immune system, are proposed to be a cause of bile duct lesions in PBC. Recent progress disclosed that cellular senescence and autophagy are involved in bile duct lesions in PBC. Senescent BECs may modulate the periductal microenvironment by expressing senescence-associated secretory phenotypes, including various chemokines, and contribute to the pathogenesis of bile duct lesions in PBC.


1980 ◽  
Vol 30 (5) ◽  
pp. 303-316
Author(s):  
KATSUHISA SUKA ◽  
SHOJI YAMADA ◽  
TOSHIKAZU SEKIGUCHI

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Motoko Sasaki ◽  
Yasuni Nakanuma

Primary biliary cirrhosis (PBC) is characterized by antimitochondrial autoantibodies (AMAs) in patients' sera and histologically by chronic nonsuppurative destructive cholangitis in small bile ducts, eventually followed by extensive bile duct loss and biliary cirrhosis. The autoimmune-mediated pathogenesis of bile duct lesions, including the significance of AMAs, triggers of the autoimmune process, and so on remain unclear. We have reported that cellular senescence in biliary epithelial cells (BECs) may be involved in bile duct lesions and that autophagy may precede the process of biliary epithelial senescence in PBC. Interestingly, BECs in damaged bile ducts show characteristicsof cellular senescence and autophagy in PBC. A suspected causative factor of biliary epithelial senescence is oxidative stress. Furthermore, senescent BECs may modulate the microenvironment around bile ducts by expressing various chemokines and cytokines called senescence-associated secretory phenotypes and contribute to the pathogenesis in PBC.


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