N-3 polyunsaturated fatty acids impede the TCR mobility and the TCR-pMHC interaction of anti-viral CD8+ T cells

Younghyun Lim, Seyoung Kim, Sehoon Kim, Dong In Kim, Kyung Won Kang, So Hee Hong, Sang Myeong Lee, Hye Ran Koh, Young Jin Seo

Research output: Contribution to journalArticlepeer-review

2 Scopus citations


The immune-suppressive effects of omega-3 (n-3) polyunsaturated fatty acids (PUFAs) on T cells have been observed via multiple in vitro and in vivo models. However, the precise mechanism that causes these effects is still undefined. In this study, we investigated whether n-3 PUFAs regulated T cell receptor (TCR) and peptide-major histocompatibility complex (pMHC) interactions. The expansion of anti-viral CD8+ T cells that endogenously synthesize n-3 PUFAs (FAT-1) dramatically decreased upon lymphocytic choriomeningitis virus (LCMV) infection in vivo. This decrease was not caused by the considerable reduction of TCR expression or the impaired chemotactic activity of T cells. Interestingly, a highly inclined and laminated optical sheet (HILO) microscopic analysis revealed that the TCR motility was notably reduced on the surface of the FAT-1 CD8+ T cells compared to the wild type (WT) CD8+ T cells. Importantly, the adhesion strength of the FAT-1 CD8+ T cells to the peptide-MHC was significantly lower than that of the WT CD8+T cells. Consistent with this result, treatment with docosahexaenoic acid (DHA), one type of n-3 PUFA, significantly decreased CD8+ T cell adhesion to the pMHC. Collectively, our results reveal a novel mechanism through which n-3 PUFAs decrease TCR-pMHC interactions by modulating TCR mobility on CD8+ T cell surfaces.

Original languageEnglish
Article numberv12060639
Issue number6
StatePublished - Jun 2020

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© 2020 by the authors.


  • CD8+ T cells
  • LCMV
  • Omega-3
  • TCR-pMHC interaction


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