| First Author | Palliser D | Year | 2004 |
| Journal | J Immunol | Volume | 172 |
| Issue | 6 | Pages | 3415-21 |
| PubMed ID | 15004140 | Mgi Jnum | J:88611 |
| Mgi Id | MGI:3036383 | Doi | 10.4049/jimmunol.172.6.3415 |
| Citation | Palliser D, et al. (2004) Myeloid differentiation factor 88 is required for cross-priming in vivo. J Immunol 172(6):3415-21 |
| abstractText | We describe a role for myeloid differentiation factor 88 (MyD88) in the induction of functional CTLs in vivo, in response to exogenously administered Ag, using a heat shock fusion protein, hsp65-P1, as a model Ag. CD8 T cells transferred into MyD88-deficient animals produce normal numbers of CD8 effector cells that have normal activation marker profiles after immunization with hsp65-P1. However, these CD8 T cells produced significantly less IFN-gamma and showed reduced killing activity. This reduction in activation of functional CTLs appears to be unrelated to Toll-like receptor 4 function, because in vitro hsp65-P1-experienced Toll-like receptor 4-deficient dendritic cells (DCs), but not MyD88-deficient DCs, activated CD8 T cells to a similar extent to wild-type DCs. We identify a cross-presentation defect in MyD88-deficient DCs that, when treated with hsp65-P1 fusion protein, results in surface display of fewer SIYRYYGL/class I MHC complexes. Thus, MyD88 plays a role in the developmental maturation of DCs that allows them to prime CD8 T cells through cross-presentation. |
