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Iron is essential for virtually all cells and higher eukaryotes due to its central role for oxygen transport, mitochondrial respiration, DNA synthesis and metabolic processes. Moreover, iron catalyses the formation of hydroxyl radicals, which can cause cellular damage but which also modulate the binding affinity of several transcription factors.1 Therefore, iron overload and iron deficiency exert subtle effects on essential metabolic pathways and on the growth, proliferation and differentiation of cells. Accordingly, iron is centrally involved in the regulation of cellular immune function. On the one hand iron promotes the proliferation and differentiation of immune cells, including lymphocytes; however, lymphocyte subsets differ in their dependence on a sufficient supply of iron. The induction of experimental iron overload in rats resulted in a shift in the ratio between T-helper (CD4+) and T-suppressor/cytotoxic T cells (CD8+) with a relative expansion of the latter.2 Moreover, T-helper (Th) subsets respond differently to iron perturbations with Th-1 cells being more sensitive to iron restriction than Th-2 cells. In addition, Th-1-mediated immune effector pathways are much more sensitive to changes in iron homeostasis in vivo.2 As with eukaryotes, microorganisms have evoked multiple strategies to capture and ingest iron, which they need for proliferation and pathogenicity while immune cells on the other hand try to restrict this essential nutrient from microbes which is a central component of host …
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