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Dynamic Cardiolipin Synthesis Is Required for CD8 T Cell Immunity. | LitMetric

AI Article Synopsis

  • Mitochondria adapt to a cell's metabolic needs, which is especially important for T cells that change their metabolism based on signals and environment.
  • * The synthesis of the mitochondrial lipid cardiolipin is essential for maintaining the function of CD8 T cells, particularly when they need to respond to antigens and for memory cell differentiation under stress.
  • * T cells lacking the enzyme PTPMT1, which helps synthesize cardiolipin, show impaired function, highlighting the importance of cardiolipin regulation in T cell immunity, especially evident in conditions like Barth syndrome.

Article Abstract

Mitochondria constantly adapt to the metabolic needs of a cell. This mitochondrial plasticity is critical to T cells, which modulate metabolism depending on antigen-driven signals and environment. We show here that de novo synthesis of the mitochondrial membrane-specific lipid cardiolipin maintains CD8 T cell function. T cells deficient for the cardiolipin-synthesizing enzyme PTPMT1 had reduced cardiolipin and responded poorly to antigen because basal cardiolipin levels were required for activation. However, neither de novo cardiolipin synthesis, nor its Tafazzin-dependent remodeling, was needed for T cell activation. In contrast, PTPMT1-dependent cardiolipin synthesis was vital when mitochondrial fitness was required, most notably during memory T cell differentiation or nutrient stress. We also found CD8 T cell defects in a small cohort of patients with Barth syndrome, where TAFAZZIN is mutated, and in a Tafazzin-deficient mouse model. Thus, the dynamic regulation of a single mitochondrial lipid is crucial for CD8 T cell immunity.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7721104PMC
http://dx.doi.org/10.1016/j.cmet.2020.11.003DOI Listing

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