Linked Life Data

12193708

Source:http://linkedlifedata.com/resource/pubmed/id/12193708

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2002-8-23
pubmed:abstractText
The liver is tolerogenic in many situations, including as an allograft and during the response to allogeneic MHC expressed on hepatocytes. The majority of data that address this issue focus on endogenous Ags. Little is known about CD4(+) T cells and their fate under tolerizing conditions, especially with respect to fully differentiated CD4(+) effector T cells. In this study, we used the adoptive transfer of populations of TCR-transgenic CD4(+) T cells, skewed toward the Th1 or Th2 phenotype, to test whether either apoptotic or immune deviation mechanisms apply to cytokine-producing CD4(+) T cells that enter the liver. After transfer, Th1 and Th2 cells could be detected up to 25 days in lymphoid organs and the liver. Intravenous high dose Ag application resulted in accumulation, proliferation, and subsequent deletion of effector cells within the liver. Th1 cells lost their capacity to produce cytokines, whereas IL-4 expression was sustained within Th2 cells from the liver. However, there was no evidence for a deviation of Th1-programmed cells toward a Th2 (IL-4) or regulatory T cell (IL-10) pattern of cytokine expression. We used isolated populations of liver-derived APCs to test whether the liver had the capacity to impose a bias toward IL-4 expression in T cells. These experiments showed that liver sinusoidal endothelial cells selectively suppress the expansion of IFN-gamma-producing cells, yet they promote the outgrowth of IL-4-expressing Th2 cells, creating an immune suppressive milieu within this organ. These data suggest that presentation of Ags in the liver leads to modulation of immune response in terms of quantity and quality.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
169
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2407-13
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:12193708-Amino Acid Sequence, pubmed-meshheading:12193708-Animals, pubmed-meshheading:12193708-CD4-Positive T-Lymphocytes, pubmed-meshheading:12193708-Cell Division, pubmed-meshheading:12193708-Cell Movement, pubmed-meshheading:12193708-Cell Survival, pubmed-meshheading:12193708-Clonal Deletion, pubmed-meshheading:12193708-Down-Regulation, pubmed-meshheading:12193708-Endothelium, Vascular, pubmed-meshheading:12193708-Immune Tolerance, pubmed-meshheading:12193708-Injections, Intravenous, pubmed-meshheading:12193708-Interferon-gamma, pubmed-meshheading:12193708-Interleukin-4, pubmed-meshheading:12193708-Liver, pubmed-meshheading:12193708-Lymphocyte Activation, pubmed-meshheading:12193708-Mice, pubmed-meshheading:12193708-Mice, Inbred BALB C, pubmed-meshheading:12193708-Mice, Knockout, pubmed-meshheading:12193708-Mice, Transgenic, pubmed-meshheading:12193708-Molecular Sequence Data, pubmed-meshheading:12193708-Ovalbumin, pubmed-meshheading:12193708-Peptide Fragments, pubmed-meshheading:12193708-Time Factors
pubmed:year
2002
pubmed:articleTitle
Immunomodulatory effects of the liver: deletion of activated CD4+ effector cells and suppression of IFN-gamma-producing cells after intravenous protein immunization.
pubmed:affiliation
Section of Immunobiology, Yale University Medical School, New Haven, CT 06520, USA. klugewitz@drfz.de
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't