Presence of disease specific autoantibodies against liver sinusoidal cells in primary biliary cirrhosis

Sfakianaki, Ourania; Tzardi, Maria; Voumvouraki, Argyro; Afgoustaki, Aikaterini; Koulentaki, Mairi

doi:10.4254/wjh.v5.i10.568

Cited by 4 publications

(3 citation statements)

References 35 publications

(41 reference statements)

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“…Endothelins also cause contraction of stellate cells thus helping in the early appearance of portal hypertension in PBC [188] . In agreement with this hypothesis are findings from our group indicating that disease specific antibodies against liver sinusoidal cells circulate in PBC [189] . In addition we reported that polymorphisms related to endothelial cells were associated with PBC.…”

Section: Pathogenesis Of Pbc: a Unifying Hypothesissupporting

confidence: 88%

Primary biliary cirrhosis: From bench to bedside

Notas

2015

WJGPT

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Primary biliary cirrhosis (PBC) is a chronic nonsuppurative destructive intrahepatic cholangitis leading to cirrhosis after a protractive non cirrhotic stage. The etiology and pathogenesis are largely unknown and autoimmne mechanisms have been implicated to explain the pathological lesions. Many epitopes and autoantigens have been reported as crucial in the pathophysiology of the disease and T and B cells abnormalities have been described, the exact pathways leading to the destruction of small intrahepatic ductules are mostly speculative. In this review we examined the various epidemiologal and geoepidemiological data as well as the complex pathogenetic aspects of this disease, focusing on recent in vivo and in vitro studies in this field. Initiation and progression of PBC is believed to be a multifactorial process with strong infuences from the patient's genetic background and by various environmental factors. The role of innate and adaptive immunity, including cytokines, chemokines, macrophages and the involvement of apoptosis and reactive oxygen species are outlined in detailed. The current pathogenetic aspects are presented and a novel pathogenetic theory unifying the accumulated clinical information with in vitro and in vivo data is formulated.A review of clinical manifestations and immunological and pathological diagnosis was presented. Treatment modalities, including the multiple mechanisms of action of ursodeoxycholate were finally discussed. Core tip: Primary biliary cirrhosis (PBC) is a chronic nonsuppurative destructive intrahepatic cholangitis leading to cirrhosis of largely unknown pathophysiology. We examined the epidemiological and geoepidemiological data as well as the pathogenetic aspects of PBC. A novel pathogenetic theory unifying the accumulated clinical information with in vitro and in vivo data is formulated.

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Section: Pathogenesis Of Pbc: a Unifying Hypothesissupporting

confidence: 88%

Primary biliary cirrhosis: From bench to bedside

Notas

2015

WJGPT

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“…An understanding of the endothelial system is essential to appreciating normal physiology but also disease processes. Changes in LSEC composition have been observed in a number of conditions such as hepatic fibrosis 3 , autoimmune disease 4 , and viral hepatitis 5 . A map of the endothelial structures in the normal liver is essential to appreciate the structural and molecular changes that take place in diseases of the liver.…”

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confidence: 99%

Immunofluorescence identifies distinct subsets of endothelial cells in the human liver

Strauß

Phillips

Ruggiero

et al. 2017

Sci Rep

131

102

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As well as systemic vascular endothelial cells, the liver has specialised sinusoidal endothelial cells (LSEC). LSEC dysfunction has been documented in many diseased states yet their phenotype in normal human liver has not been comprehensively assessed. Our aim was to improve characterisation of subsets of endothelial cells and associated pericytes in the human liver. Immunofluorescence microscopy was performed on normal human liver tissue samples to assess endothelial and structural proteins in a minimum of three donors. LSEC are distributed in an acinar pattern and universally express CD36, but two distinctive subsets of LSEC can be identified in different acinar zones. Type 1 LSEC are CD36hiCD32−CD14−LYVE-1− and are located in acinar zone 1 of the lobule, while Type 2 LSEC are LYVE-1+CD32hiCD14+CD54+CD36mid-lo and are located in acinar zones 2 and 3 of the lobule. Portal tracts and central veins can be identified using markers for systemic vascular endothelia and pericytes, none of which are expressed by LSEC. In areas of low hydrostatic pressure LSEC are lined by stellate cells that express the pericyte marker CD146. Our findings identify distinctive populations of LSEC and distinguish these cells from adjacent stellate cells, systemic vasculature and pericytes in different zones of the liver acinus.

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“…Changes in LSEC composition have been observed in a number of conditions such as hepatic fibrosis 3 , autoimmune disease 4 , and viral hepatitis 5 . A map of the endothelial structures in the normal liver is essential to appreciate the structural and molecular changes that take place in diseases of the liver.…”

Section: As Well As Systemic Vascular Endothelial Cells the Liver Hamentioning

confidence: 99%

Immunofluorescence identifies distinct subsets of endothelial cells in the human liver

Strauß¹,

Phillips²,

Ruggiero³

et al. 2017

Journal of Hepatology

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Presence of disease specific autoantibodies against liver sinusoidal cells in primary biliary cirrhosis

Abstract: AIM:To investigate the presence of autoantibodies directed against liver sinusoidal cells in primary biliary cirrhosis (PBC).

Cited by 4 publications

References 35 publications

Primary biliary cirrhosis: From bench to bedside

Primary biliary cirrhosis: From bench to bedside

Immunofluorescence identifies distinct subsets of endothelial cells in the human liver

Immunofluorescence identifies distinct subsets of endothelial cells in the human liver

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