Abstract
SummaryVaccination programmes are critically important to suppress the burden of infectious diseases, saving countless lives globally, as emphasised by the current COVID-19 pandemic. Effective adaptive immune responses are complex processes subject to multiple influences. Recent genetic, pre-clinical, and clinical studies have converged to show that availability of iron is a key factor regulating the development of T and B cell responses to infection and immunisation. Lymphocytes obtain iron from circulating transferrin. The amount of iron bound to transferrin is dependent on dietary iron availability and is decreased during inflammation via upregulation of the iron-regulatory hormone, hepcidin. As iron deficiency and chronic inflammatory states are both globally prevalent health problems, the potential impact of low iron availability on immune responses is significant. We describe the evidence supporting the importance of iron in immunity, highlight important unknowns, and discuss how therapeutic interventions to modulate iron availability might be implementable in the context of vaccination and infectious disease.
Highlights
Our group recently demonstrated that transient acute serum iron deficiency, driven physiologically through enhanced hepcidin activity, suppresses the antigen-specific CD8, CD4, and B cell immune response in mice [42]
In piglets, a natural model of iron deficiency, we found that responses to vaccination were improved by iron interventions that increased serum iron [42]
This review focuses on iron deficiency, we should note that genetic diseases which suppress hepcidin and lead to systemic iron loading have been proposed to influence immunity
Summary
The study by Jabara et al.[43] demonstrates that adaptive immune responses require iron, the influence of variable serum iron availability on immune cells remained unaddressed. Our group recently demonstrated that transient acute serum iron deficiency, driven physiologically through enhanced hepcidin activity, suppresses the antigen-specific CD8, CD4, and B cell immune response in mice [42].
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