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15096489

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

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pubmed-article:15096489pubmed:abstractTextTransforming 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.lld:pubmed
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pubmed-article:15096489pubmed:articleTitleMechanisms 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.lld:pubmed
pubmed-article:15096489pubmed:affiliationDepartment of Microbiology and Immunology, University of Louisville Health Sciences Center, Louisville, KY 40202, USA. mmkosi01@gwise.louisville.edulld:pubmed
pubmed-article:15096489pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:15096489pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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