title: The role of vitamin E in T-cell differentiation and the decrease of cellular immunity with aging.
abstract: Spontaneously hypertensive rats (SHR) as a model for aging were used in this experiment and fed a regular (50 IU/Kg diet) or high vitamin E (500 IU/Kg diet) diet for 6 weeks. At 12 weeks old, they were killed and assayed. Although proliferation of thymic lymphocytes was significantly decreased in SHR fed the regular diet compared to Wistar Kyoto rats (WKY) fed the same diet, high vitamin E diet enhanced proliferation of thymic lymphocytes in SHR to almost the levels in WKY fed the regular diet. In addition, the expressions of both CD4 and CD8 antigens on CD+CD8+ T cells, immature T cells existing in thymic cortex, were also decreased in SHR, and significantly improved by high vitamin E diet. These results suggest that high vitamin E diet enhances thymic lymphocyte proliferation through increased T-cell differentiation in thymus. Then, the effect of vitamin E on T-cell differentiation in thymus was investigated by using male Fisher rats. Rats were divided into three groups; vitamin E-free, regular and high vitamin E groups and fed a diet containing various levels of vitamin E (0, 50 and 500 IU/Kg diet) for 7 weeks. Although the percentages of CD4+CD8- and CD4-CD8+ T cells in thymocytes were significantly greater in the high vitamin E group, the percentage of CD4+CD8- T cells inversely decreased in the vitamin E-free group compared to the regular group. We have tried to investigate the mechanism of the increased T-cell differentiation in thymus of rats fed the high vitamin E diet through cytokine production, and thymic epithelial cell (TEC) and macrophage functions. We have found that vitamin E enhances T-cell differentiation through the increase of not macrophage but TEC function in thymus, which is associated with the increased binding capacity of TEC to immature T cells via increased expression of adhesion molecule, ICAM-1. These results suggest that vitamin E is a potent nutrient for promoting health in the aged via the improvement of cellular immunity decreased with aging.
authors.affiliation: Department of Nutrition, University of Tokushima School of Medicine, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Moriguchi
authors.forename: M
authors.initials: M
authors.lastname: Hamada
authors.forename: K
authors.initials: K
authors.lastname: Yamauchi
authors.forename: K
authors.initials: K
authors.lastname: Sakai
authors.forename: S
authors.initials: S
authors.lastname: Yamamoto
mesh_terms: D000375:Aging / Q000276:immunology*; D000818:Animals; D002448:Cell Adhesion; D002454:Cell Differentiation; D004032:Diet; D004847:Epithelial Cells / Q000502:physiology; D007111:Immunity, Cellular / Q000502:physiology*; D018799:Intercellular Adhesion Molecule-1 / Q000502:physiology; D008264:Macrophages / Q000502:physiology; D008297:Male; D011833:Radiation Injuries, Experimental / Q000276:immunology; D051381:Rats; D011916:Rats, Inbred F344; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D016176:T-Lymphocyte Subsets / Q000166:cytology* / Q000378:metabolism; D013950:Thymus Gland / Q000166:cytology* / Q000254:growth & development / Q000528:radiation effects; D014810:Vitamin E / Q000502:physiology*
chemical_list: D018799:Intercellular Adhesion Molecule-1; D014810:Vitamin E