Ferroptosis of T cell in inflammation and tumour immunity

Abstract Ferroptosis is an innovative concept defined as a distinct programmed cell death mode regulated by iron‐dependent lipid peroxidation accumulation. This process is governed by numerous energy metabolites such as fatty acids, amino acids and glucose, as well as iron homeostasis. In recent years, increasing studies have been devoted to the crucial effects of ferroptosis in immune cells during the pathogenesis of diseases such as infections, tumours and autoimmune disorders. This review summarises the latest advancements in T‐cell ferroptosis, addresses the key components and mechanism of ferroptosis in T cells during inflammatory conditions and tumour progression, and highlights the potential target for treating related diseases. Key points Ferroptosis‐related mechanisms significantly affect the biology of CD4 + T‐cell subsets and are further involved in inflammatory diseases. Crosstalk between CD8 + T cells and tumour cells induces ferroptosis in the tumour microenvironment. Glutathione peroxidase 4 loss promotes regulatory T‐cell ferroptosis to enhance anti‐tumour immunity.