The potential role of interleukin-2 in impaired cell-mediated immunity of iron deficiency
Helyar, Lesley
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Permalink
https://hdl.handle.net/2142/20250
Description
Title
The potential role of interleukin-2 in impaired cell-mediated immunity of iron deficiency
Author(s)
Helyar, Lesley
Issue Date
1991
Department of Study
Nutritional Sciences
Discipline
Nutritional Sciences
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(s)
Biology, Cell
Biology, Microbiology
Health Sciences, Nutrition
Language
eng
Abstract
Iron deficiency impairs cell-mediated immunity, which is primarily dependent on T-lymphocyte functions including production of the cytokine, interleukin 2 (IL-2). The potential role of IL-2 production and responsiveness in impaired cell-mediated immunity of iron deficiency was investigated in a series of experiments. Immune parameters were measured in unstimulated and concanavalin A (Con A)-stimulated spleen lymphocytes from rats and mice. Dietary iron deficiency induced in the weanling Sprague-Dawley rat and C57/B16 mouse were used as the nutritional models.
Severe, but not moderate iron deficiency, impaired lymphocyte production of IL-2 by rat spleen lymphocytes. In severe iron deficiency, there were lower numbers of T-lymphocytes, and these cells did not become normally activated and divide in response to Con A. The effect of iron deficiency on responsiveness of lymphocytes to IL-2 varied with the parameter of cell-mediated immunity studied. The responsiveness of T-cytotoxicity against P815 mastocytoma cells to IL-2 stimulation was quantitatively and qualitatively normal in iron deficiency with moderate anemia; T-cytotoxicity was not impaired. Natural killer cell activity responsiveness to IL-2 in iron deficiency was lower compared to responsiveness in normal iron status. Attempts to restore blastogenesis with in iron-deficient spleen lymphocytes with IL-2 were unsuccessful, although quantitative and qualitative responses to IL-2 were normal, the rate of cell proliferation in iron-deficiency remained lower than the control rate.
Cell cycle progression to division was also impeded in iron deficiency. Additional study of cell surface activation markers showed that iron deficiency decreased the expression of one marker, the Ia antigen, but did not decrease the proportion of IL-2 receptor-positive cells. Results from studies combining both immune cell activation and subset determinations indicated that there are decreased numbers of mature B-lymphocytes cells in Con A-stimulated spleen lymphocytes of iron-deficient animals, but that Con A stimulation appeared to normalize the phenotypic expression of T-lymphocyte and T-lymphocyte subset markers. Despite the apparent normalization of T-lymphocyte phenotype by Con A stimulation in iron deficiency, there were fewer T-lymphocytes that became activated in response to Con A stimulation. In severe iron deficiency, but not moderate iron deficiency, activation of B-lymphocytes was also lower compared with normal iron status.
In iron deficiency there are smaller numbers of mature lymphocytes, and these lymphocytes do not become activated and divide as readily as normal lymphocytes. This may explain decreased IL-2 production and the limitation in response to IL-2 stimulation observed.
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