Protein keeps resting immune cells' metabolism quiet in mice
After infection, mouse immune cells lacking the protein expanded an average of 70 times between days 5 and 8, versus 120 times for normal cells.
Limit: The functional experiments used gene deletion; raising the protein was not measured
Stake: Medical Genomics funded the study.
Edited by Boris Djordjevic · AgingResearch.News
In experiments in male and female mice, researchers studied naive CD8 T cells, immune cells that had not yet encountered their target. They deleted the gene for AFF3, a protein that regulates gene activity, in T cells. They transferred equal numbers of CD8 T cells with and without AFF3 into the same mice before infecting them with a virus.
Before infection, cells lacking AFF3 had more active metabolism, the chemical processes that supply energy and materials. After infection, they accumulated less. This was linked to a poorer ability to engage glycolysis, the breakdown of sugar for energy. AFF3 gene activity was lower in CD8 T cells from mice older than 12 months than in those younger than 5 months. AFF3 expression also declined with aging in human CD8 T cells.
Why it matters
Immune cells lose metabolic restraint as their responses to infection weaken with age. The authors identified AFF3 as a possible target for reinvigorating CD8 T cell responses during aging.
Caveats
The functional experiments used gene deletion in mice; the human finding concerned gene activity, not improved immunity. These results do not establish whether raising AFF3 would help older people.
The paper
AFF3 maintains metabolic quiescence in naive CD8 T cells and prevents premature immune aging
Indiana University Melvin and Bren Simon Comprehensive Cancer Center
JCI Insight, Jun 23, 2026, Open access
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