Please use this identifier to cite or link to this item: https://doi.org/10.4049/jimmunol.1801585
Title: The Lysophosphatidylcholine Transporter MFSD2A Is Essential for CD8(+) Memory T Cell Maintenance and Secondary Response to Infection
Authors: Piccirillo, Ann R
Hyzny, Eric J
Beppu, Lisa Y
Menk, Ashley V
Wallace, Callen T
Hawse, William F
Buechel, Heather M
Wong, Bernice H
Foo, Juat Chin 
Cazenave-Gassiot, Amaury
Wenk, Markus R 
Delgoffe, Greg M
Watkins, Simon C
Silver, David L
D'Cruz, Louise M
Keywords: Science & Technology
Life Sciences & Biomedicine
Immunology
FATTY-ACIDS
EFFECTOR
METABOLISM
ACTIVATION
RECEPTORS
EXPRESSION
SUPPORT
PROTEIN
BRAIN
GLUT1
Issue Date: 1-Jul-2019
Publisher: AMER ASSOC IMMUNOLOGISTS
Citation: Piccirillo, Ann R, Hyzny, Eric J, Beppu, Lisa Y, Menk, Ashley V, Wallace, Callen T, Hawse, William F, Buechel, Heather M, Wong, Bernice H, Foo, Juat Chin, Cazenave-Gassiot, Amaury, Wenk, Markus R, Delgoffe, Greg M, Watkins, Simon C, Silver, David L, D'Cruz, Louise M (2019-07-01). The Lysophosphatidylcholine Transporter MFSD2A Is Essential for CD8(+) Memory T Cell Maintenance and Secondary Response to Infection. JOURNAL OF IMMUNOLOGY 203 (1) : 117-126. ScholarBank@NUS Repository. https://doi.org/10.4049/jimmunol.1801585
Abstract: © 2019 by The American Association of Immunologists, Inc. Access to nutrients is critical for an effective T cell immune response to infection. Although transporters for sugars and amino acids have previously been described in the context of the CD8+ T cell immune response, the active transport of exogenous fatty acids has remained enigmatic. In this study, we discovered that the sodium-dependent lysophosphatidylcholine (LPC) transporter major facilitator superfamily domain containing 2A (MFSD2A) is upregulated on activated CD8+ T cells and is required for memory T cell maintenance. MFSD2A deficiency in mice resulted in decreased import of LPC esterified to long chain fatty acids into activated CD8+ T cells, and MFSD2A-deficient cells are at a competitive disadvantage resulting in reduced memory T cell formation and maintenance and reduced response to secondary infection. Mechanistically, import of LPCs was required to maintain T cell homeostatic turnover, which when lost resulted in a decreased memory T cell pool and thus a reduced secondary response to repeat infection.
Source Title: JOURNAL OF IMMUNOLOGY
URI: https://scholarbank.nus.edu.sg/handle/10635/173175
ISSN: 00221767
15506606
DOI: 10.4049/jimmunol.1801585
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