| First Author | Okoye I | Year | 2015 |
| Journal | Science | Volume | 348 |
| Issue | 6238 | Pages | 995-1001 |
| PubMed ID | 25883318 | Mgi Jnum | J:223336 |
| Mgi Id | MGI:5648685 | Doi | 10.1126/science.aaa7516 |
| Citation | Okoye I, et al. (2015) T cell metabolism. The protein LEM promotes CD8(+) T cell immunity through effects on mitochondrial respiration. (Expression of Concern 350 (6267): 1482). Science 348(6238):995-1001 |
| abstractText | AP has kept this retracted publication because it is the original description for two mutant alleles that are not described elsewhere. The reason for retraction does not involve the construction of the mutant mice. "Protective CD8(+) T cell-mediated immunity requires a massive expansion in cell number and the development of long-lived memory cells. Using forward genetics in mice, we identified an orphan protein named lymphocyte expansion molecule (LEM) that promoted antigen-dependent CD8(+) T cell proliferation, effector function, and memory cell generation in response to infection with lymphocytic choriomeningitis virus. Generation of LEM-deficient mice confirmed these results. Through interaction with CR6 interacting factor (CRIF1), LEM controlled the levels of oxidative phosphorylation (OXPHOS) complexes and respiration, resulting in the production of pro-proliferative mitochondrial reactive oxygen species (mROS). LEM provides a link between immune activation and the expansion of protective CD8(+) T cells driven by OXPHOS and represents a pathway for the restoration of long-term protective immunity based on metabolically modified cytotoxic CD8(+) T cells. |
