Iron Deficiency in Immune-Mediated Inflammatory Skin Diseases: A Missing Link Between Systemic Inflammation, Immunometabolism, and Disease Burden
March 2026
in “
Cells
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iron deficiency immune-mediated inflammatory skin diseases psoriasis atopic dermatitis hidradenitis suppurativa IL-6 hepcidin iron sequestration mitochondrial activity oxidative responses anemia of chronic disease epidermal keratinocytes iron homeostasis systemic inflammation immunometabolic imbalance
Studysummary This review highlights that iron deficiency is a significant yet often overlooked contributor to the development of immune-mediated inflammatory skin diseases, suggesting that iron dysregulation may drive inflammation and metabolic imbalances in conditions like psoriasis and atopic dermatitis.
Our plain-language summary. Not medical advice or a treatment recommendation. Consult a qualified healthcare professional before changing treatment. Full disclaimer
Iron deficiency (ID) is a critical factor in the development of immune-mediated inflammatory skin diseases (IMISDs) like psoriasis and atopic dermatitis, due to its role in systemic inflammation and immunometabolism. Chronic inflammation, mediated by the IL-6-hepcidin axis, leads to functional iron deficiency by sequestering iron and reducing its bioavailability, which impairs mitochondrial function, immune regulation, and tissue repair. This imbalance exacerbates oxidative stress and inflammation, contributing to disease chronicity. The review introduces the concept of an "iron-skin axis," where keratinocytes regulate iron pathways, influencing local inflammation. Conventional iron supplementation is often ineffective in these conditions, suggesting the need for targeted therapeutic strategies focusing on the hepcidin-ferroportin axis. Understanding iron regulation's impact on inflammation and disease progression could lead to better patient outcomes in chronic IMISDs.
