| First Author | Correa-Medero LO | Year | 2024 |
| Journal | Cell Rep | Volume | 43 |
| Issue | 5 | Pages | 114156 |
| PubMed ID | 38687642 | Mgi Jnum | J:349788 |
| Mgi Id | MGI:7658763 | Doi | 10.1016/j.celrep.2024.114156 |
| Citation | Correa-Medero LO, et al. (2024) ER-associated degradation adapter Sel1L is required for CD8(+) T cell function and memory formation following acute viral infection. Cell Rep 43(5):114156 |
| abstractText | The maintenance of antigen-specific CD8(+) T cells underlies the efficacy of vaccines and immunotherapies. Pathways contributing to CD8(+) T cell loss are not completely understood. Uncovering the pathways underlying the limited persistence of CD8(+) T cells would be of significant benefit for developing novel strategies of promoting T cell persistence. Here, we demonstrate that murine CD8(+) T cells experience endoplasmic reticulum (ER) stress following activation and that the ER-associated degradation (ERAD) adapter Sel1L is induced in activated CD8(+) T cells. Sel1L loss limits CD8(+) T cell function and memory formation following acute viral infection. Mechanistically, Sel1L is required for optimal bioenergetics and c-Myc expression. Finally, we demonstrate that human CD8(+) T cells experience ER stress upon activation and that ER stress is negatively associated with improved T cell functionality in T cell-redirecting therapies. Together, these results demonstrate that ER stress and ERAD are important regulators of T cell function and persistence. |
