| First Author | Endo Y | Year | 2019 |
| Journal | Nat Metab | Volume | 1 |
| Issue | 2 | Pages | 261-275 |
| PubMed ID | 32694782 | Mgi Jnum | J:319335 |
| Mgi Id | MGI:6863750 | Doi | 10.1038/s42255-018-0025-4 |
| Citation | Endo Y, et al. (2019) ACC1 determines memory potential of individual CD4(+) T cells by regulating de novo fatty acid biosynthesis. Nat Metab 1(2):261-275 |
| abstractText | Immunological memory is central to adaptive immunity and protection from disease. Changing metabolic demands as antigen-specific T cells transition from effector to memory cells have been well documented, but the cell-specific pathways and molecules that govern this transition are poorly defined. Here we show that genetic deletion of ACC1, a rate-limiting enzyme in fatty acid biosynthesis, enhances the formation of CD4(+) T memory cells. ACC1-deficient effector helper T (Th) cells have similar metabolic signatures to wild-type memory Th cells, and expression of the gene encoding ACC1, Acaca, was inversely correlated with a memory gene signature in individual cells. Inhibition of ACC1 function enhances memory T cell formation during parasite infection in mice. Using single-cell analyses we identify a memory precursor-enriched population (CCR7(hi)CD137(lo)) present during early differentiation of effector CD4(+) T cells. Our data indicate that fatty acid metabolism directs cell fate determination during the generation of memory CD4(+) T cells. |
