Lipid metabolism drives dietary effects on T cell ferroptosis and immunity

"Ferroptosis, a major mechanism of non-apoptotic programmed cell death, critically regulates the homeostasis and functionality of peripheral CD4+ and CD8+ T cells. Here we demonstrate that in mouse, resistance of T cells to ferroptosis depends critically on the composition of standard rodent diets, and that dietary effects on ferroptosis have a crucial role in regulation of T cell homeostasis and immune responses."

"DEFs are microbiota-independent and are driven by variations in dietary polyunsaturated and monounsaturated fatty acids (PUFAs and MUFAs) that lead to variations in abundant lipid species, which directly influence T cell ferroptosis susceptibility."

Ferroptosis, a form of non-apoptotic programmed cell death, plays a crucial role in maintaining peripheral CD4+ and CD8+ T cell homeostasis and function. Research demonstrates that T cell resistance to ferroptosis depends significantly on standard rodent diet composition. Dietary effects on ferroptosis operate independently of the microbiota and are driven by variations in polyunsaturated and monounsaturated fatty acids. These dietary variations alter the abundance of specific lipid species, which directly influence T cell ferroptosis susceptibility and subsequently regulate T cell homeostasis and immune responses.

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