Deficiency and Immunity

Proliferation of cells requires iron, as the DNA synthetic enzyme ribonucleotide reductase is iron dependent. Impaired T cell proliferation and impaired delayed type hypersensitivity have been consistently reported in iron deficiency. Phagocytosis is accompanied by the generation of toxic oxygen intermediates to kill ingested bacteria and both neutrophils and macrophages require iron for this process - nitroblue tetrazolium reduction and hydrogen peroxide production are reduced in neu-trophils and macrophages if made iron deficient. In contrast, excessive iron results in decreased phagocytosis by neutrophils possibly due to increased free radical production and consequent lipid peroxidation damage of the phagosome membrane. Iron overload and saturation of transferrin also inhibits lymphocyte proliferation. When assessing the effect of iron on the immune system macrophages deserve special attention, as they are responsible for recycling heme iron back to the bone marrow. Iron thus fluxes through macrophages en route to fulfil hemopoietic need and is also utilized to kill intramacrophagal microbes. Macrophage activation and intracellular killing are dependent on the generation of toxic oxidant molecules such as the hydroxyl radical; however, these same free radicals can damage host cell membranes through lipid peroxidation. The control of intracellular iron in macrophages is thus important to hemopoiesis, microbial killing, and cell membrane stability within the macrophage itself. Iron overloading of macrophages impairs normal function and may increase risk of disease. Iron overloading of the macrophage causes oxidant damage to the phagocyte and an impaired ability to kill intracellular pathogens via IFN7-mediated pathways. Iron has a direct inhibitory effect on the actions of IFN-7, e.g., formation of tumor necrosis factor apha (TNF-a), expression of major histocompatibility factor (MHC) class II antigens, formation of neopterin, and nitric oxide synthesis.

Studies of immune function in iron-deficient human populations are frequently confounded by coexisting nutritional deficiencies, prevailing socioeconomic conditions, and differing diagnostic criteria, which make them difficult to interpret and compare. Increased morbidity from infectious disease has been reported in iron-deficient populations; however, it is not clear whether this is due to iron deficiency alone or at what level of deficiency the immune system is functionally compromised. In studies of children in predominately malarious areas a definite increase in mortality has only been demonstrated in anemic patients with less than 50gl 1 hemoglobin, whereas in those children with milder anemia the evidence for increased risk of mortality is inconclusive.

Zinc promotes mRNA stability, regulates gene expression, and influences DNA replication ensuring an essential role in cell division and activation. These processes are central to the immune response and zinc deficiency affects immune function at many levels both in the innate and specific arms. Zinc deficiency rarely occurs alone and has no pathogno-monic clinical features. Cell-mediated immunity is profoundly affected in zinc deficiency. Lymphopenia is common, as are defects in specific T and B lymphocyte function. Lymphoid atrophy, decreased delayed cutaneous hypersensitivity responses, reduction in numbers of CD4 helper cells, B cell dysfunction, impairment of phagocytosis, and deficient thymic hormone activity have all been described. Secretion and function of cytokines and the poten-tiation of apoptosis are affected by zinc deficiency. Gastrointestinal barrier function, polymorphonuc-lear and natural killer cell function, and complement activity are also affected. Zinc may also prevent free radical-induced injury through its antioxidant and cell membrane stabilizing properties. Mild zinc deficiency resulted in an imbalance between TH1 and TH2 functions in male volunteers - reduced serum thymulin activity, reduced CD4/CD8 lymphocyte ratio, and reduced interleukin-2 (IL-2) production but production of IL-4, IL-5, IL-6, and IL-10 was unaffected. Influencing TH1/TH2 balance is a potentially important pathway by which zinc deficiency affects cell-mediated immunity.

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