Linked Life Data

9973395

Source:http://linkedlifedata.com/resource/pubmed/id/9973395

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1999-4-13
pubmed:abstractText
Endotoxin is physiologically present in portal venous blood at concentrations of 100 pg/ml to 1 ng/ml. Clearance of endotoxin from portal blood occurs through sinusoidal lining cells, i.e., Kupffer cells, and liver sinusoidal endothelial cells (LSEC). We have recently shown that LSEC are fully efficient APCs. Here, we studied the influence of endotoxin on the accessory function of LSEC. Incubation of Ag-presenting LSEC with physiological concentrations of endotoxin lead to >/=80% reduction of the accessory function, measured by release of IFN-gamma from CD4+ T cells. In contrast, conventional APC populations rather showed an increase of the accessory function after endotoxin treatment. Inhibition of the accessory function in LSEC by endotoxin was not due to lack of soluble costimulatory signals, because neither supplemental IL-1beta, IL-2, IFN-gamma, or IL-12 could rescue the accessory function. Ag uptake was not influenced by endotoxin in LSEC. However, we found that endotoxin led to alkalinization of the endosomal/lysomal compartment specifically in LSEC but not in bone marrow macrophages, which indicated that Ag processing, i.e., proteolytic cleavage of protein Ags into peptide fragments, was affected by endotoxin. Furthermore, endotoxin treatment down-regulated surface expression of constitutively expressed MHC class II, CD80, and CD86. In conclusion, it is conceivable that endotoxin does not alter the clearance function of LSEC to remove gut-derived Ags from portal blood but specifically affects Ag processing and expression of the accessory molecules in these cells. Consequently, Ag-specific immune responses by CD4+ T cells are efficiently down-regulated in the hepatic microenvironment.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
162
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1401-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9973395-Animals, pubmed-meshheading:9973395-Antigen Presentation, pubmed-meshheading:9973395-Antigen-Presenting Cells, pubmed-meshheading:9973395-Antigens, CD, pubmed-meshheading:9973395-Antigens, CD80, pubmed-meshheading:9973395-Antigens, CD86, pubmed-meshheading:9973395-Cytokines, pubmed-meshheading:9973395-Endosomes, pubmed-meshheading:9973395-Endothelium, Vascular, pubmed-meshheading:9973395-Endotoxins, pubmed-meshheading:9973395-Female, pubmed-meshheading:9973395-Histocompatibility Antigens Class II, pubmed-meshheading:9973395-Hydrogen-Ion Concentration, pubmed-meshheading:9973395-Liver, pubmed-meshheading:9973395-Lymphocyte Activation, pubmed-meshheading:9973395-Lysosomes, pubmed-meshheading:9973395-Membrane Glycoproteins, pubmed-meshheading:9973395-Mice, pubmed-meshheading:9973395-Mice, Inbred BALB C, pubmed-meshheading:9973395-Mice, Transgenic, pubmed-meshheading:9973395-Receptors, Antigen, T-Cell, alpha-beta, pubmed-meshheading:9973395-T-Lymphocytes
pubmed:year
1999
pubmed:articleTitle
Endotoxin down-regulates T cell activation by antigen-presenting liver sinusoidal endothelial cells.
pubmed:affiliation
First Medizinische Klinik und Poliklinik, Johannes Gutenberg Universität, Mainz, Germany. P.Knolle@zmbh.uni-heidelberg.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't