Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 40, Issue 7, Pages 2006-2015Publisher
WILEY-BLACKWELL
DOI: 10.1002/eji.200939387
Keywords
CD4(+) CD25(+) T Cells; Contact hypersensitivity; DC
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Funding
- National Institutes of Health [RO1 AI45888]
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Recent studies have suggested Fas-mediated elimination of antigen-presenting cells as an important mechanism down-regulating the induction of autoimmune responses. It remains unknown whether this mechanism restricts the magnitude of immune responses to non-self antigens. We used a mouse model of a cutaneous CD8(+) T-cell-mediated immune response (contact hypersensitivity, CHS) to test if CD4(+)CD25(+) T cells expressing FasL regulate hapten-specific effector CD8(+) T cell expansion through the elimination of Fas-expressing hapten-presenting DC. In WT mice, attenuation of CD4(+)CD25(+) T regulatory cell activity by anti-CD25 mAb increased hapten-presenting DC numbers in skin-draining LN, which led to increased effector CD8(+) T-cell priming for CHS responses. In contrast, CD4(+)CD25(+) T cells did not regulate hapten-specific CD8(+) T-cell priming and CHS responses initiated by Fas-defective (lpr) DC. Thus, restricting DC priming functions through Fas-FasL interactions is a potent mechanism employed by CD4(+)CD25(+) regulatory cells to restrict CD8(+) T-cell-mediated allergic immune responses in the skin.
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