Linked Life Data

1955777

Source:http://linkedlifedata.com/resource/pubmed/id/1955777

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3-4
pubmed:dateCreated
1992-1-2
pubmed:abstractText
ASGPR may play a role in the pathogenesis of autoimmune chronic liver diseases. Several lines of evidence support this hypothesis. Antibodies to rabbit ASGPR could be found in various inflammatory liver diseases. In contrast, ASGPR preparations derived from human liver (h-ASGPR) were recognized predominantly by sera from patients with ai-CAH. Moreover, anti-h-ASGPR showed a close correlation to the inflammatory activity of ai-CAH both in terms of prevalence (88% in histologically proven active diseases), immunoglobulin class (IgM antibodies restricted to active inflammation) and behavior during treatment. Anti-h-ASGPR secretion could also be found in vitro, when PBL of patients were stimulated in cell culture. Anti-h-ASGPR antibodies did not correlate with a subgroup of ai-CAH; they also occurred in nearly 15% of patients with PBC. Other inflammatory liver diseases, as well as nonhepatic autoimmune disorders, seldom exhibited anti-h-ASGPR (less than 5%). Additionally, PBL and T-cell clones obtained from liver biopsies in patients with ai-CAH and PBC responded to h-ASGPR. Liver-infiltrating T cells were predominantly of CD4 phenotype and HLA class II restricted. Thus, the human ASGPR has been shown to represent a common target for humoral and cellular autoimmune response in chronic hepatitis probably contributing to disease induction or perpetuation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0257-277X
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
497-502
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Human asialoglycoprotein receptor as an autoantigen in chronic hepatitis.
pubmed:affiliation
First Department of Internal Medicine, Johannes Gutenberg University, Mainz, FRG.
pubmed:publicationType
Journal Article