Iron metabolism is critical to the regulation of immune system cell functions, and disruption of these processes is associated with the development of a number of diseases. This review addresses the mechanisms underlying the metabolism of iron ions at the cellular level, as well as the effects of the peptide hormone hepcidin, which regulates iron efflux from cells. The synthesis of hepcidin and its target, the iron exporter protein ferroportin, is effectively controlled by proinflammatory cytokines and stimulation of Toll-like receptors. The role of iron ions and hepcidin in regulating the functions of innate and adaptive immunity cells is defined. Specifically, iron levels influences neutrophil differentiation in the bone marrow, their phagocytic and bactericidal activity, and the formation of extracellular traps. Hepcidin-mediated regulation of the intracellular iron levels modulates macrophage polarization and their production of proinflammatory cytokines, as well as the cytotoxic activity of NK cells. Iron ions are required for the activation and proliferation of T and B lymphocytes; they modulate the differentiation of effector subpopulations of helper and cytotoxic T lymphocytes, the formation of memory B cells, and antibody production. The review highlights the role of iron ions and hepcidin during pregnancy, as iron is essential for placental and fetal development, as well as maternal adaptation to pregnancy. Thus, the study of the relationship between iron metabolism and the functions of immune system cells is of profound fundamental and practical significance. Targeting iron metabolism offers a new promising approach to the treatment of infectious, oncological, and neurodegenerative diseases, as well as conditions associated with impaired iron homeostasis during pregnancy.
Orlova et al. (2026) studied this question.