| First Author | Welten SP | Year | 2015 |
| Journal | Elife | Volume | 4 |
| PubMed ID | 26263500 | Mgi Jnum | J:269501 |
| Mgi Id | MGI:6207724 | Doi | 10.7554/eLife.07486 |
| Citation | Welten SP, et al. (2015) The viral context instructs the redundancy of costimulatory pathways in driving CD8(+) T cell expansion. Elife 4 |
| abstractText | Signals delivered by costimulatory molecules are implicated in driving T cell expansion. The requirements for these signals, however, vary from dispensable to essential in different infections. We examined the underlying mechanisms of this differential T cell costimulation dependence and found that the viral context determined the dependence on CD28/B7-mediated costimulation for expansion of naive and memory CD8(+) T cells, indicating that the requirement for costimulatory signals is not imprinted. Notably, related to the high-level costimulatory molecule expression induced by lymphocytic choriomeningitis virus (LCMV), CD28/B7-mediated costimulation was dispensable for accumulation of LCMV-specific CD8(+) T cells because of redundancy with the costimulatory pathways induced by TNF receptor family members (i.e., CD27, OX40, and 4-1BB). Type I IFN signaling in viral-specific CD8(+) T cells is slightly redundant with costimulatory signals. These results highlight that pathogen-specific conditions differentially and uniquely dictate the utilization of costimulatory pathways allowing shaping of effector and memory antigen-specific CD8(+) T cell responses. |
