| First Author | Corrado M | Year | 2020 |
| Journal | Cell Metab | Volume | 32 |
| Issue | 6 | Pages | 981-995.e7 |
| PubMed ID | 33264603 | Mgi Jnum | J:300251 |
| Mgi Id | MGI:6489767 | Doi | 10.1016/j.cmet.2020.11.003 |
| Citation | Corrado M, et al. (2020) Dynamic Cardiolipin Synthesis Is Required for CD8(+) T Cell Immunity. Cell Metab 32(6):981-995.e7 |
| abstractText | 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. |
