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Acc1 determines memory potential of individual CD4+ T cells by regulating de novo fatty acid biosynthesis

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE122863 | GEO | 2018/11/30

REPOSITORIES: GEO

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Acc1 determines memory potential of individual CD4+ T cells by regulating de novo fatty acid biosynthesis [microarray]

Project description:Immunological memory is central to adaptive immunity and protection from disease. Changing metabolic demands as antigen-specific T cells transition from effector to memory have been well documented, but the cell-specific pathways and molecules that govern this transition are poorly defined. ACC1 is a rate-limiting enzym in fatty acid biosynthesis. We show that genetic deletion of ACC1 enhanced the formation of CD4+ T cell memory, and that inhibition of ACC1 function enhanced memory T cell formation during parasite infection in mice. ACC1-deficient effector Th cells had similar metabolic signatures to wild-type memory Th cells, and Acaca expression was inversely correlated with a memory gene signature in individual cells. Single cell analysis allowed us to identify a memory precursor-enriched population (CCR7hiCD137lo) present during early differentiation of effector CD4+ T cells. Thus, fatty acid metabolism directs cell fate determination during the generation of memory CD4+ T cells.

2018-11-30 | GSE122861 | GEO

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Acc1 determines memory potential of individual CD4+ T cells by regulating de novo fatty acid biosynthesis [RT-PCR]

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