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J Immunol. 2019 Jul 1;203(1):117-126. doi: 10.4049/jimmunol.1801585. Epub 2019 May 24.

The Lysophosphatidylcholine Transporter MFSD2A Is Essential for CD8+ Memory T Cell Maintenance and Secondary Response to Infection.

Author information

1
Department of Immunology, University of Pittsburgh, Pittsburgh, PA 15213.
2
Tumor Microenvironment Center, UPMC Hillman Cancer Center, Pittsburgh, PA 15232.
3
Center for Biologic Imaging, University of Pittsburgh, Pittsburgh, PA 15213.
4
Signature Research Program in Cardiovascular and Metabolic Diseases, Duke-National University of Singapore Graduate Medical School, Singapore 159857, Singapore; and.
5
Department of Biochemistry, National University of Singapore, Singapore 117597, Singapore.
6
Department of Immunology, University of Pittsburgh, Pittsburgh, PA 15213; ldcruz@pitt.edu.

Abstract

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.

PMID:
31127034
PMCID:
PMC6581627
[Available on 2020-07-01]
DOI:
10.4049/jimmunol.1801585

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