New research shows that dietary iron deficiency impairs antiviral immunity in the lungs and the effects may persist even after iron levels return to normal (Figure 1).
Figure 1: Mouse model of dietary iron deficiency. (A) Weight curves by weeks on iron defined diets for each cohort; boxes represent mean with bars representing standard deviation. (B) Comparison of hemoglobin by group at weeks 4 and 5 on defined diets. Bars represent mean and range with boxes depicting interquartile range. (C) Quantification of liver iron at diet week 5 for each cohort, box with bars represents mean with standard deviation. For all panels, n = 5 mice per group. All statistical testing via Mann–Whitney t test. ** = P < 0.01, *** = P < 0.001, **** = P < 0.0001.
A recent study reveals that iron deficiency during infection can leave a lasting mark on the immune system, reducing the ability of lung T cells to fight off viruses such as influenza. The findings may help explain why iron deficiency, one of the world’s most common nutritional problems, is linked to conditions like asthma and recurrent respiratory infections.
Iron deficiency disproportionately affects women, infants, and young children, yet its impact on immune development has been poorly understood. This new research shows that when iron levels are low during infection, lung immune cells fail to produce interferon-gamma, a critical antiviral signal. Even more striking:
Restoring iron levels later did not fix the problem.
This suggests that iron deficiency during key moments of infection may cause long-term functional changes in lung immune memory.
The team studied memory T cells, immune cells that stay in lung tissue after infection and respond rapidly if the virus returns.
Mice were fed either an iron-rich or iron-deficient diet before being infected with influenza. While memory T cells formed in both groups, only the iron-sufficient mice produced normal, functional T cells capable of secreting interferon-gamma. In iron-deficient mice, the lung T cells looked normal but failed to activate properly.
The defect was:
- Specific to the lungs, not other tissues
- Not reversible, even when cells were later exposed to iron-rich conditions
The study suggests that iron deficiency during respiratory infections may weaken long-term immunity, leaving individuals more vulnerable to future viral illnesses. It also opens the door to understanding how poor iron status may contribute to chronic airway conditions.
Dietary iron deficiency during infection impairs the lung’s ability to build strong immune memory, a defect that may persist even after iron levels normalize. Ensuring adequate iron intake could be essential for improving antiviral immunity and long-term respiratory health.
Journal article: Bradley, M.C., et al. 2025. Dietary iron deficiency impairs effector function of memory T cells following influenza infection. The Journal of Immunology.
Summary by Stefan Botha
