Ferroptosis is a regulated form of cell death characterized by lipid peroxidation and iron dependency. It plays a critical role in immune-related diseases, including infection, autoimmune disorders, and cancer. This review discusses the mechanisms of ferroptosis, its regulation in immune cells, and its implications for disease pathogenesis. Ferroptosis is regulated by a complex interplay between death-promoting signals and defense systems, including glutathione peroxidase 4 (GPX4) and system xc-. GPX4 is essential for preventing lipid oxidation and cell death, while system xc- imports cystine, which is converted to cysteine to synthesize glutathione (GSH), an important antioxidant. Ferroptosis can be induced by pro-inflammatory cytokines, fatty acids, and other factors, and is inhibited by ferroptosis inhibitors such as ferrostatin-1 and liproxstatin-1. Ferroptosis is also regulated by other factors, including the mitochondrial pathway, endoplasmic reticulum (ER), and lysosomes. The role of ferroptosis in immune homeostasis is increasingly recognized, with implications for immune cell function, tumor immunity, and autoimmune diseases. Ferroptosis can be modulated by various factors, including iron, cystine, and lipid metabolism. Targeting ferroptosis may offer new therapeutic strategies for cancer and autoimmune diseases. The review highlights the importance of understanding ferroptosis in the context of immune-related diseases and its potential for clinical translation.Ferroptosis is a regulated form of cell death characterized by lipid peroxidation and iron dependency. It plays a critical role in immune-related diseases, including infection, autoimmune disorders, and cancer. This review discusses the mechanisms of ferroptosis, its regulation in immune cells, and its implications for disease pathogenesis. Ferroptosis is regulated by a complex interplay between death-promoting signals and defense systems, including glutathione peroxidase 4 (GPX4) and system xc-. GPX4 is essential for preventing lipid oxidation and cell death, while system xc- imports cystine, which is converted to cysteine to synthesize glutathione (GSH), an important antioxidant. Ferroptosis can be induced by pro-inflammatory cytokines, fatty acids, and other factors, and is inhibited by ferroptosis inhibitors such as ferrostatin-1 and liproxstatin-1. Ferroptosis is also regulated by other factors, including the mitochondrial pathway, endoplasmic reticulum (ER), and lysosomes. The role of ferroptosis in immune homeostasis is increasingly recognized, with implications for immune cell function, tumor immunity, and autoimmune diseases. Ferroptosis can be modulated by various factors, including iron, cystine, and lipid metabolism. Targeting ferroptosis may offer new therapeutic strategies for cancer and autoimmune diseases. The review highlights the importance of understanding ferroptosis in the context of immune-related diseases and its potential for clinical translation.