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 esterified fatty acids has remained enigmatic. Here we discovered the long chain fatty acid transporter, Major Facilitator Super Family Domain Containing 2a (MFSD2A), is upregulated on activated CD8+ T cells and is essential for their memory cell formation. MFSD2A deficiency resulted in decreased import of long chain fatty acids (LCFAs) esterified to lysophosphatidylcholine (LPC) into activated CD8+ T cells but overall resulted in a normal primary effector T cell response. However, loss of MFSD2A led to reduced memory T cell formation and maintenance. MFSD2A deficient memory CD8+ T cells showed reduced CD127 and CD62L expression and their cell turnover was significantly impaired in contrast to their wildtype counterparts. Moreover, the secondary response to infection was severely diminished in MFSD2A deficient T cells. Mechanistically, import of LCFAs was required to maintain cell energy requirements and ‘fitness’, that when lost resulted in a decreased memory T cell pool and inability to proliferate upon secondary stimulation. Our results show that MFSD2A and LPC may be useful for future small molecule therapy design to generate a more robust T cell response for new vaccines or cancer treatments.