Linked Life Data

15265953

Source:http://linkedlifedata.com/resource/pubmed/id/15265953

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2004-7-21
pubmed:abstractText
A subset of CD161(+)CD56(+/-) NKT cells can recognize glycolipids presented by CD1d and positively or negatively regulate inflammatory responses, including those implicated in several models of hepatitis. CD1d is expressed at very low levels in the healthy liver, but there is a large fraction of CD161(+)CD56(+) NKT cells. There are high levels of nonclassical proinflammatory hepatic CD1d-reactive T cells in hepatitis C virus (HCV) infection. Hepatic inflammatory cells and biliary cells adjacent to portal tract fibrotic areas of HCV-infected donors specifically up-regulated CD1d. A hepatocyte cell line expressing minimal CD1d was efficiently recognized by hepatic CD1d-reactive T cells, suggesting a role for these cells in disease. Hepatic CD1d-reactive T cells from HCV-positive as well as negative donors produced large amounts of IFN-gamma with some IL-13, but only rarely detectable IL-4. We confirmed large numbers of hepatic CD161(+) T cells, lower levels of CD56(+) T cells, and small numbers of classic invariant NKT cells. However, hepatic CD1d-reactivity was not restricted to any of these populations. We suggest virally infected hepatic cells can process potent CD1d-presented liver Ag(s), for surveillance by resident Th1 hepatic CD1d-reactive T cells. This process may be beneficial in acute viral clearance, but in chronic infection could contribute to liver injury.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
173
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2159-66
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:15265953-Acute Disease, pubmed-meshheading:15265953-Antigen Presentation, pubmed-meshheading:15265953-Antigens, CD1, pubmed-meshheading:15265953-Antigens, CD1d, pubmed-meshheading:15265953-Antigens, CD56, pubmed-meshheading:15265953-Antigens, Surface, pubmed-meshheading:15265953-Cell Line, pubmed-meshheading:15265953-Gene Expression Regulation, pubmed-meshheading:15265953-Hepatitis C, pubmed-meshheading:15265953-Hepatitis C, Chronic, pubmed-meshheading:15265953-Hepatocytes, pubmed-meshheading:15265953-Humans, pubmed-meshheading:15265953-Interferon-gamma, pubmed-meshheading:15265953-Interleukin-13, pubmed-meshheading:15265953-Killer Cells, Natural, pubmed-meshheading:15265953-Lectins, C-Type, pubmed-meshheading:15265953-Liver, pubmed-meshheading:15265953-Liver Cirrhosis, pubmed-meshheading:15265953-Models, Immunological, pubmed-meshheading:15265953-NK Cell Lectin-Like Receptor Subfamily B, pubmed-meshheading:15265953-T-Lymphocyte Subsets, pubmed-meshheading:15265953-Th1 Cells, pubmed-meshheading:15265953-Th2 Cells, pubmed-meshheading:15265953-Transfection
pubmed:year
2004
pubmed:articleTitle
Hepatic CD1d expression in hepatitis C virus infection and recognition by resident proinflammatory CD1d-reactive T cells.
pubmed:affiliation
Infectious Diseases Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't