Linked Life Data

15096489

Source:http://linkedlifedata.com/resource/pubmed/id/15096489

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2004-5-3
pubmed:abstractText
Transforming growth factor (TGF)-beta-treated antigen-presenting cells [(APC) adherent peritoneal exudate cells] induce a profound tolerance in primed mice that is thought to be mediated by regulatory T cells induced in the spleen. In the current study, we investigated the mechanism(s) involved in tolerance induced in primed mice by TGF-beta-treated APC. Interestingly, TGF-beta-treated APC from class II knockout mice were unable to mediate tolerance in primed mice and failed to induce not only CD4, but also CD8 regulatory T cells. However, the results of several experiments indicated that it was the CD8 regulatory T cells that were required for tolerance induced in primed mice. Using neutralizing antibody, we found that TGF-beta-treated APC-induced CD8 regulatory T cells did not suppress effector T cell function in vivo through the production of IL-4, TGF-beta or IL-10. On the other hand, our data showed that the Fas-Fas ligand (FasL) pathway was involved in this form of tolerance since TGF-beta-treated APC could not mediate tolerance in primed FasL-deficient mice and CD8 T cells from FasL-deficient mice were unable to suppress effector T cell responses. Moreover, the targets of FasL-mediated suppression were found to be the effector T cells as suggested by the data showing that Fas-deficient effector T cells were not susceptible to suppression mediated by CD8 regulatory T cells induced by TGF-beta-treated APC. In conclusion, our data indicate that TGF-beta-treated APC effect tolerance in primed mice via a Fas-FasL-mediated mechanism that requires CD8 cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0953-8178
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
697-706
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:15096489-Animals, pubmed-meshheading:15096489-Antigen-Presenting Cells, pubmed-meshheading:15096489-CD4-Positive T-Lymphocytes, pubmed-meshheading:15096489-Fas Ligand Protein, pubmed-meshheading:15096489-Female, pubmed-meshheading:15096489-Genes, MHC Class II, pubmed-meshheading:15096489-Hypersensitivity, Delayed, pubmed-meshheading:15096489-Immune Tolerance, pubmed-meshheading:15096489-Immunization, pubmed-meshheading:15096489-Interleukin-10, pubmed-meshheading:15096489-Interleukin-4, pubmed-meshheading:15096489-Lymphocyte Depletion, pubmed-meshheading:15096489-Membrane Glycoproteins, pubmed-meshheading:15096489-Mice, pubmed-meshheading:15096489-Mice, Knockout, pubmed-meshheading:15096489-Ovalbumin, pubmed-meshheading:15096489-T-Lymphocytes, Regulatory, pubmed-meshheading:15096489-Transforming Growth Factor beta
pubmed:year
2004
pubmed:articleTitle
Mechanisms of tolerance induced by transforming growth factor-beta-treated antigen-presenting cells: CD8 regulatory T cells inhibit the effector phase of the immune response in primed mice through a mechanism involving Fas ligand.
pubmed:affiliation
Department of Microbiology and Immunology, University of Louisville Health Sciences Center, Louisville, KY 40202, USA. mmkosi01@gwise.louisville.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.