Liver · 2000
Fas ligand expressing mononuclear cells around intrahepatic bile ducts co-express CD68 in primary biliary cirrhosis.
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Iwata M, Harada K, Hiramatsu K, Tsuneyama K, Kaneko S, Kobayashi K, Nakanuma Y
Аннотация
AIMS/BACKGROUND: Apoptosis, including the Fas system, has been implicated in progressive bile duct loss in primary biliary cirrhosis (PBC). In this study, we attempted to analyze Fas ligand (FasL) expressing mononuclear cells infiltrating in the portal tracts of PBC.
METHODS: We immunohistochemically assessed co-expression of leukocyte markers and FasL on infiltrating mononuclear cells in 18 patients with PBC. Twenty-five patients with chronic hepatitis C (CH-C) were used as controls.
RESULTS: In PBC, FasL expressing cells were scattered in the portal tracts, and some were accentuated around the damaged bile ducts. In addition, these cells co-expressed CD68 (71%), a marker of monocytes, but not UCHL-1, CD3 and CD57, markers of activated T cells and natural killer cells. By contrast, in CH-C, the biliocentric pattern of FasL expression was not evident, and about half of FasL expressing cells (42-56%) co-expressed UCHL-1, CD3 or CD57. CD14, a receptor for bacterial products such as lipopolysaccharides, was also detected on a proportion of FasL expressing mononuclear cells around the damaged bile ducts in PBC.
CONCLUSION: The results suggest that in PBC, FasL expressing CD68+ monocytes are at least partly involved in apoptotic bile duct loss mediated by the Fas system, and a surface molecule, CD14, participates in this process.
METHODS: We immunohistochemically assessed co-expression of leukocyte markers and FasL on infiltrating mononuclear cells in 18 patients with PBC. Twenty-five patients with chronic hepatitis C (CH-C) were used as controls.
RESULTS: In PBC, FasL expressing cells were scattered in the portal tracts, and some were accentuated around the damaged bile ducts. In addition, these cells co-expressed CD68 (71%), a marker of monocytes, but not UCHL-1, CD3 and CD57, markers of activated T cells and natural killer cells. By contrast, in CH-C, the biliocentric pattern of FasL expression was not evident, and about half of FasL expressing cells (42-56%) co-expressed UCHL-1, CD3 or CD57. CD14, a receptor for bacterial products such as lipopolysaccharides, was also detected on a proportion of FasL expressing mononuclear cells around the damaged bile ducts in PBC.
CONCLUSION: The results suggest that in PBC, FasL expressing CD68+ monocytes are at least partly involved in apoptotic bile duct loss mediated by the Fas system, and a surface molecule, CD14, participates in this process.