BibTex format
@article{Sheppard:2024:10.1073/pnas.2319254121,
author = {Sheppard, S and Srpan, K and Lin, W and Lee, M and Delconte, RB and Owyong, M and Carmeliet, P and Davis, DM and Xavier, JB and Hsu, KC and Sun, JC},
doi = {10.1073/pnas.2319254121},
journal = {Proceedings of the National Academy of Sciences of USA},
title = {Fatty acid oxidation fuels natural killer cell responses against infection and cancer},
url = {http://dx.doi.org/10.1073/pnas.2319254121},
volume = {121},
year = {2024}
}
RIS format (EndNote, RefMan)
TY - JOUR
AB - Natural killer (NK) cells are a vital part of the innate immune system capable of rapidly clearing mutated or infected cells from the body and promoting an immune response. Here, we find that NK cells activated by viral infection or tumor challenge increase uptake of fatty acids and their expression of carnitine palmitoyltransferase I (CPT1A), a critical enzyme for long-chain fatty acid oxidation. Using a mouse model with an NK cell-specific deletion of CPT1A, combined with stable 13C isotope tracing, we observe reduced mitochondrial function and fatty acid-derived aspartate production in CPT1A-deficient NK cells. Furthermore, CPT1A-deficient NK cells show reduced proliferation after viral infection and diminished protection against cancer due to impaired actin cytoskeleton rearrangement. Together, our findings highlight that fatty acid oxidation promotes NK cell metabolic resilience, processes that can be optimized in NK cell-based immunotherapies.
AU - Sheppard,S
AU - Srpan,K
AU - Lin,W
AU - Lee,M
AU - Delconte,RB
AU - Owyong,M
AU - Carmeliet,P
AU - Davis,DM
AU - Xavier,JB
AU - Hsu,KC
AU - Sun,JC
DO - 10.1073/pnas.2319254121
PY - 2024///
SN - 0027-8424
TI - Fatty acid oxidation fuels natural killer cell responses against infection and cancer
T2 - Proceedings of the National Academy of Sciences of USA
UR - http://dx.doi.org/10.1073/pnas.2319254121
UR - https://www.ncbi.nlm.nih.gov/pubmed/38442180
UR - https://www.pnas.org/doi/10.1073/pnas.2319254121
UR - http://hdl.handle.net/10044/1/111693
VL - 121
ER -