Linked Life Data

8552995

Source:http://linkedlifedata.com/resource/pubmed/id/8552995

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1996-2-20
pubmed:abstractText
The influence of lipopolysaccharide (LPS) and various cytokines on the expression of the costimulatory molecule B7-1 and intercellular adhesion molecule-1 (ICAM-1), lymphocyte function associated antigen-3 (LFA-3) and human histocompatibility leucocyte antigen-DR (HLA-DR) on human monocytes and their effect on the costimulatory function was investigated. Freshly isolated human monocytes constitutively express ICAM-1, LFA-3 and HLA-DR, but no B7-1. B7-1 expression was up-regulated by LPS and, to a lesser extent, by interferon-gamma (IFN-gamma). The other stimuli tested, including IFN-alpha, granulocyte-macrophage colony-stimulating factor (GM-CSF), tumour necrosis factor-alpha (TNF-alpha) and GM-CSF+TNF-alpha, did not influence expression of B7-1 on monocytes. ICAM-1 and HLA-DR were up-regulated by IFN-gamma and LPS; LFA-3 expression was not influenced. LPS also effectively enhanced costimulatory function of monocytes as determined in the tetanustoxoid (TT) assay. Blocking of B7 by CTLA-4Ig inhibited the LPS-induced enhancement of costimulatory function almost completely. Our results indicate that the LPS-mediated up-regulation of the costimulatory function of human monocytes is mediated by B7. This mechanism may be important for host defence against Gram-negative bacteria.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0300-9475
pubmed:author
pubmed:issnType
Print
pubmed:volume
42
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
701-4
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Lipopolysaccharide effectively up-regulates B7-1 (CD80) expression and costimulatory function of human monocytes.
pubmed:affiliation
Department of Hematology Oncology, Medizinische Klinik V, University of Heidelberg, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't