| First Author | Ehrlich LI | Year | 2005 |
| Journal | J Immunol | Volume | 174 |
| Issue | 4 | Pages | 1922-31 |
| PubMed ID | 15699119 | Mgi Jnum | J:155163 |
| Mgi Id | MGI:4412369 | Doi | 10.4049/jimmunol.174.4.1922 |
| Citation | Ehrlich LI, et al. (2005) Engagement of NKG2D by cognate ligand or antibody alone is insufficient to mediate costimulation of human and mouse CD8+ T cells. J Immunol 174(4):1922-31 |
| abstractText | CD8+ T cells require a signal through a costimulatory receptor in addition to TCR engagement to become activated. The role of CD28 in costimulating T cell activation is well established. NKG2D, a receptor found on NK cells, CD8+ alphabeta-TCR+ T cells, and gammadelta-TCR+ T cells, has also been implicated in T cell costimulation. In this study we have evaluated the role of NKG2D in costimulating mouse and human naive and effector CD8+ T cells. Unexpectedly, in contrast to CD28, NKG2D engagement by ligand or mAb is not sufficient to costimulate naive or effector CD8+ T cell responses in conventional T cell populations. While NKG2D did not costimulate CD8+ T cells on its own, it was able to modify CD28-mediated costimulation of human CD8+ T cells under certain contitions. It is, therefore, likely that NKG2D acts as a costimulatory molecule only under restricted conditions or requires additional cofactors. |
