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L. M. Allende, A. Corell, A. Madrono, R. Gongora, C. Rodriguez-Gallego, A. Lopez-Goyanes, M. Rosal and A. Arnaiz-Villena, “Retinol (Vitamin A) Is a Cofactor in CD3-Induced Human T-Lymphocyte Activation,” Immunology, Vol. 90, No. 3, 1997, pp. 388-396.
doi:10.1111/j.1365-2567.1997.00388.x
has been cited by the following article:
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TITLE:
Alteration in T-Cell Cytokine Production by Vitamin A and Zinc Supplementation in Mice
AUTHORS:
Sorayya Kheirvari, Mohammad Alizadeh
KEYWORDS:
Zinc; Vitamin A; IgA; IL-5; IL-2; IFN-γ
JOURNAL NAME:
Food and Nutrition Sciences,
Vol.3 No.8,
August
8,
2012
ABSTRACT: Simultaneous zinc and vitamin A deficiency are common health problems in developing countries. The objective of this study was to assess effect of supplementation of high zinc or vitamin A on immune function. After three months of feeding with a zinc and vitamin A deficient diet, mice were assigned into four groups which, for additional two months, received a normal or high zinc along with vitamin A deficient diet and a normal or high vitamin A along with zinc deficient diet. Serum and intestinal mucosa immunoglobulin A (IgA) were determined and supernatants of splenocytes were used to assess interlukin (IL)-2, IL-5, IFN-γ. Mice maintained on zinc deficient diet with normal or high vitamin A resulted in significantly lower production of IFN-γ. Also, supplementation of high dose vitamin A augmented production of the cytokine as compared to normal intake of the vitamin. Supplementation of either normal or high zinc along with low vitamin A diet significantly led to higher production of IFN-γ as compared to those receiving zinc limited but adequate vitamin A. High intake of zinc along with vitamin A deficient diet significantly enhanced secretion of IL-2. Levels of serum and mucosal IgA and IL-5 were not be significantly modulated. Moreover, animals fed with high doses of zinc showed increased IL-2 production than those that had normal intake of zinc. Results indicated that zinc and vitamin A supplementation up-regulates production of T-cell cytokines, IFN-γ and IL-2.