| First Author | Yang J | Year | 2016 |
| Journal | Oncotarget | Volume | 7 |
| Issue | 23 | Pages | 33744-64 |
| PubMed ID | 27014906 | Mgi Jnum | J:301585 |
| Mgi Id | MGI:6506278 | Doi | 10.18632/oncotarget.8164 |
| Citation | Yang J, et al. (2016) Unexpected positive control of NFkappaB and miR-155 by DGKalpha and zeta ensures effector and memory CD8+ T cell differentiation. Oncotarget 7(23):33744-64 |
| abstractText | Signals from the T-cell receptor (TCR) and gamma-chain cytokine receptors play crucial roles in initiating activation and effector/memory differentiation of CD8 T-cells. We report here that simultaneous deletion of both diacylglycerol kinase (DGK) alpha and zeta (DKO) severely impaired expansion of CD8 effector T cells and formation of memory CD8 T-cells after Listeria monocytogenes infection. Moreover, ablation of both DGKalpha and zeta in preformed memory CD8 T-cells triggered death and impaired homeostatic proliferation of these cells. DKO CD8 T-cells were impaired in priming due to decreased expression of chemokine receptors and migration to the draining lymph nodes. Moreover, DKO CD8 T-cells were unexpectedly defective in NFkappaB-mediated miR-155 transcript, leading to excessive SOCS1 expression and impaired gamma-chain cytokine signaling. Our data identified a DGK-NFkappaB-miR-155-SOCS1 axis that bridges TCR and gamma-chain cytokine signaling for robust CD8 T-cell primary and memory responses to bacterial infection. |
