| First Author | Gorbachev AV | Year | 2004 |
| Journal | J Immunol | Volume | 172 |
| Issue | 4 | Pages | 2286-95 |
| PubMed ID | 14764697 | Mgi Jnum | J:88048 |
| Mgi Id | MGI:3029055 | Doi | 10.4049/jimmunol.172.4.2286 |
| Citation | Gorbachev AV, et al. (2004) CD4(+) T cells regulate CD8(+) T cell-mediated cutaneous immune responses by restricting effector T cell development through a Fas ligand-dependent mechanism. J Immunol 172(4):2286-95 |
| abstractText | The magnitude and duration of CD8(+) T cell-mediated responses in the skin to hapten sensitization and challenge, contact hypersensitivity (CHS), is negatively regulated by CD4(+) T cells through an unknown mechanism. In this study we show that CD4(+) T cells restrict the development and expansion of hapten-specific CD8(+) T cells mediating CHS responses to 2,4-dinitrofluorobenzene. In the absence of CD4(+) T cells, high numbers of hapten-specific CD8(+) T cells producing IFN-gamma were detected in the skin-draining lymph nodes on day 5 postsensitization, and these numbers decreased slightly, but were maintained through day 9, correlating with the increased magnitude and duration of CHS responses observed in these mice. In the presence of CD4(+) T cells, the number of hapten-specific CD8(+) T cells producing IFN-gamma detected on day 5 postsensitization was lower and quickly fell to background levels by day 7. The limited development of effector CD8(+) T cells was associated with decreased numbers of hapten-presenting dendritic cells in the lymphoid priming site. This form of immunoregulation was absent after sensitization of Fas ligand-defective gld mice. Transfer of wild-type CD4(+) T cells to gld mice restored the negative regulation of CD8(+) T cell priming and the immune response to hapten challenge in gld-recipient mice. These results indicate that CD4(+) T cells restrict hapten-specific CD8(+) T cell priming for CHS responses through a Fas ligand-dependent mechanism. |
