Effect of dietary high doses of vitamin E on lymphocyte subsets in young and old CBA mice.
Different theories of ageing exist. Oxidative stress by generating neo-antigens and affecting cellular communications may precipitate immune disregulation, and both may concur in the whole ageing process. In the present study, we have analysed the effect of dietary high doses of vitamin E, a free radical scavenger, on blood and spleen leukocytes and lymphocyte subsets, in young (3-month-old) and old (23-month-old) CBA mice. Age per se induced an increase in blood leukocytes, especially phagocytic cells, and a splenic atrophy, affecting both weight and cellularity. A differential effect of age on blood or spleen lymphocyte subsets was observed. In blood, there was a decrease in T cells, particularly CD4+ cells (T helper cells) and CD5+ cells without surface IgM (conventional T cells), along with a corresponding increase in B cells, principally B1 CD5+ cells (polyreactive autoimmunity-prone B cells). In the spleen, the relative percentage of each subset remained unchanged. Vitamin E supplementation for 7 weeks before sacrifice in young animals resulted in a decrease in CD4+ and CD5+ SIgM+ (putative Fc-receptor positive) T cells and B1 cells in blood. Similar changes in the splenic lymphocyte subsets were found, while more leukocytes could be recovered from less weighty spleens. Considering the free radical scavenging properties of vitamin E, it was assumed that oxidative stress might play some role in the ontogenesis of the immune system in young adulthood. Vitamin E for 20 months before sacrifice in old animals did not prevent splenic atrophy and had no effect on splenocytes. In blood, the ratio of SIgM+ (assumed Fc-R+) to SIgM- CD5+ T cells decreased and the B1:B2 B-cell ratio increased. In this setting, oxidative stress seemed to play a lesser role in post-adulthood immune senescence. It must be stressed that no functional test was realized that could have uncovered qualitative changes in immune reactivity. Vitamin E supplementation had complex effects on the weight of our animals, so that influences on physical activity, energy metabolism and hormonal status should be considered in interpreting its impact on the immune system. However, the observed age-related changes in T-cell and B-cell subsets are consistent with diminished immune function and increased autoimmunity in senescence. Vitamin E, by a direct anti-oxidant effect or some other mechanisms, can prevent some changes and seems to decrease the potential for autoimmune reactivity.
Brohée
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Laboratory of Experimental Medicine (U.L.B.), C.H.U. André Vésale, Montigny-le-Tilleul, Belgium.
Nève
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D000375:Aging / Q000097:blood* / Q000276:immunology; D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D015551:Autoimmunity / Q000187:drug effects; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects / Q000276:immunology; D018956:CD5 Antigens; D005260:Female; D016166:Free Radical Scavengers / Q000008:administration & dosage; D007075:Immunoglobulin M / Q000378:metabolism; D016131:Lymphocyte Subsets / Q000187:drug effects* / Q000276:immunology; D008297:Male; D051379:Mice; D008808:Mice, Inbred CBA; D018384:Oxidative Stress / Q000187:drug effects; D011947:Receptors, Antigen, B-Cell / Q000378:metabolism; D013154:Spleen / Q000166:cytology / Q000187:drug effects / Q000276:immunology; D014810:Vitamin E / Q000008:administration & dosage*
D015703:Antigens, CD; D018956:CD5 Antigens; D016166:Free Radical Scavengers; D007075:Immunoglobulin M; D011947:Receptors, Antigen, B-Cell; D014810:Vitamin E