| First Author | Gorbachev AV | Year | 2010 |
| Journal | Eur J Immunol | Volume | 40 |
| Issue | 7 | Pages | 2006-15 |
| PubMed ID | 20405474 | Mgi Jnum | J:161865 |
| Mgi Id | MGI:4461832 | Doi | 10.1002/eji.200939387 |
| Citation | Gorbachev AV, et al. (2010) CD4(+)CD25(+) regulatory T cells utilize FasL as a mechanism to restrict DC priming functions in cutaneous immune responses. Eur J Immunol 40(7):2006-2015 |
| abstractText | 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. |
