Linked Life Data

11673481

Source:http://linkedlifedata.com/resource/pubmed/id/11673481

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pubmed-article:11673481pubmed:abstractTextBlocking the CD28/B7 and/or CD154/CD40 costimulatory pathways promotes long-term allograft survival in many transplant models where CD4(+) T cells are necessary for rejection. When CD8(+) T cells are sufficient to mediate rejection, these approaches fail, resulting in costimulation blockade-resistant rejection. To address this problem we examined the role of lymphotoxin-related molecules in CD8(+) T cell-mediated rejection of murine intestinal allografts. Targeting membrane lymphotoxin by means of a fusion protein, mAb, or genetic mutation inhibited rejection of intestinal allografts by CD8(+) T cells. This effect was associated with decreased monokine induced by IFN-gamma (Mig) and secondary lymphoid chemokine (SLC) gene expression within allografts and spleens respectively. Blocking membrane lymphotoxin did not inhibit rejection mediated by CD4(+) T cells. Combining disruption of membrane lymphotoxin and treatment with CTLA4-Ig inhibited rejection in wild-type mice. These data demonstrate that membrane lymphotoxin is an important regulatory molecule for CD8(+) T cells mediating rejection and suggest a strategy to avoid costimulation blockade-resistant rejection.lld:pubmed
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pubmed-article:11673481pubmed:articleTitleCutting edge: membrane lymphotoxin regulates CD8(+) T cell-mediated intestinal allograft rejection.lld:pubmed
pubmed-article:11673481pubmed:affiliationEmory Transplant Center and Department of Surgery, Emory University School of Medicine, Atlanta, GA 30322, USA.lld:pubmed
pubmed-article:11673481pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11673481pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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