Abstract
Differentiation of T cells is closely associated with dynamic changes in nutrient and energy metabolism. However, the extent to which specific metabolic pathways and molecular components are determinative of CD8+ T cell fate remains unclear. It has been previously established in various tissues that acetyl CoA carboxylase 2 (ACC2) regulates fatty acid oxidation (FAO) by inhibiting carnitine palmitoyltransferase 1 (CPT1), a rate-limiting enzyme of FAO in mitochondria. Here, we explore the cell-intrinsic role of ACC2 in T cell immunity in response to infections. We report here that ACC2 deficiency results in a marginal increase of cellular FAO in CD8+ T cells, but does not appear to influence antigen-specific effector and memory CD8+ T cell responses during infection with listeria or lymphocytic choriomeningitis virus. These results suggest that ACC2 is dispensable for CD8+ T cell responses.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Acetyl-CoA Carboxylase / genetics
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Acetyl-CoA Carboxylase / immunology*
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Animals
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CD8-Positive T-Lymphocytes / enzymology
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CD8-Positive T-Lymphocytes / immunology*
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Carnitine O-Palmitoyltransferase / genetics
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Carnitine O-Palmitoyltransferase / immunology
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Carnitine O-Palmitoyltransferase / metabolism
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Fatty Acids / genetics
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Fatty Acids / immunology
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Fatty Acids / metabolism
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Immunity, Cellular*
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Listeria monocytogenes / immunology
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Listeriosis / enzymology
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Listeriosis / genetics
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Listeriosis / immunology
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Lymphocytic Choriomeningitis / enzymology
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Lymphocytic Choriomeningitis / genetics
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Lymphocytic Choriomeningitis / immunology
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Lymphocytic choriomeningitis virus / immunology
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Mice
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Mice, Transgenic
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Mitochondria / enzymology
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Mitochondria / genetics
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Mitochondria / immunology*
Substances
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Fatty Acids
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Carnitine O-Palmitoyltransferase
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Acacb protein, mouse
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Acetyl-CoA Carboxylase