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Vitamin E and T cell development

With the importance of vitamin E adequacy to a strong immune system so clearly demonstrated, much of the research on the subject is now exploring the modes of action that are involved.

In work with broilers at the University of Arkansas, Erf et al. (1998) shed more light on the relationship between vitamin E status and the development of T cells, leukocytes that develop mainly in the thymus but also in the spleen. This work involved 1,900 male broiler chicks whose diet from hatch through seven weeks of age included four treatment levels of vitamin E supplementation: 0; 15,454; 41,818; or 79,090 IU per ton of feed (0, 17, 46 or 87 IU/kg). The highest level of supplementation was roughly three to five times the level found in many commercial broiler operations, the authors noted.

T cells' immune functions include both direct destruction of antigens and the activation of other immune cells. However, these functions belong to two separate subpopulations of T cells, commonly called killer and helper cells, which differentiate as they mature.

Killer T cells destroy specific target cells, primarily virus-infected and tumor cells. Helper T cells, by contrast, produce chemicals (cytokines) that activate B cells, macrophages and killer T cells, and also influence the class of antibody produced by the B cells. Thus, while less directly lethal to antigens, helper T cells have a more central function in regulating the immune response than killer T cells.

Erf et al. (1998) reported increases in both the percentage of T cells that had developed into helper cells and the percentage of all T cells that were mature with increased dietary vitamin E supplementation (P < 0.05). An increase in the total percentage of T cells that are mature is important because immature T cells undergo selection processes that result in the death of more than 95 percent of these cells before they differentiate into functioning helper or killer cells.

In seven-week-old broilers receiving the highest vitamin E supplementation, fully 29.5 percent of the T cells in the thymus were mature, capable of performing the helper or killer function (Figure 1). In unsupplemented birds, by contrast, mature T cells accounted for only 18.6 percent of the total T cell population at seven weeks of age. For the intermediate treatments, total mature T cell populations in the thymus at seven weeks of age increased as the vitamin E level increased.

 

Figure 1

This difference by vitamin E treatment was all the more notable because the researchers reported no significant differences by treatment at two weeks of age. Thus, in the broilers receiving the highest level of supplementation, the mature T cell population at seven weeks had increased by two-thirds over the population at two weeks of age. In the birds receiving no supplementation, the population at seven weeks was only one fifth greater than at two weeks.

Virtually all the significant differences by treatment in the thymus T cell populations involved the helper T cell subpopulation. For example, helper T cells accounted for 20.7 percent of the total T cell population in broilers receiving the highest level of dietary vitamin E supplementation, but only 11.4 percent in the broilers receiving no supplementation (Figure 2).

 

Figure 2

There was also a significant (P < 0.05) increase in helper T cell populations with the highest level of supplementation compared to birds receiving a typical commercial level of vitamin E supplementation.

Compared with populations at two weeks of age, the helper T cell population increased by 118 percent in the broilers receiving the highest level of vitamin E supplementation. In those receiving no vitamin E the helper T cell population increased by only 29 percent.

Cell population analysis of the spleen at seven weeks of age also showed a significant increase (P < 0.05) in helper T cells in the birds receiving the highest level of supplementation compared to all other treatments. Helper T cells were 7.7 percent of all splenocytes with the highest level of vitamin E, whereas they ranged between 4.7 and 5.3 percent for the other three treatments.

The results in this study agree with those in previous work by Erf and Bottje (1996), which found a greater ratio of helper to killer T cells as dietary vitamin E supplementation increased. In that work, T cell proliferation in response to mitogenic stimulation was also significantly greater with increased vitamin E supplementation.

Erf et al. (1998) suggested that the antioxidant properties of vitamin E may play a role in cell survival within the thymus. Work with human lymphocytes (Duthie et al., 1996) provided evidence that vitamin E decreases oxidative DNA damage, and work with mice (Forrest  et al., 1994) indicated that vitamin E decreased oxidative stress-induced fragmentation of thymic T cells.

Modes of action to explain the effects of vitamin E status on immunocompetence are not mutually exclusive, of course. In the meantime, Erf and Bottje (1996) noted that "evidence for immune enhancing effects of vitamin E supplementation continues to accumulate, demonstrating beneficial effects of vitamin E on immunity to coccidiosis, E. coli, Newcastle disease and infectious bursal disease."

Erf et al., (1998) added: "Considering the central immunomodulatory role of these cells, together with the variety of immunological challenges broilers are exposed to at a very young age, it would appear that additional dietary vitamin E supplementation may be beneficial to the overall immunocompetence of growing broilers."

 

References:

  • Duthie, S.J., et al., 1996. Antioxidant supplementation decreases oxidative DNA damage in human lymphocytes. Cancer Res. 56:1291.
  • Erf, G.F., et al., 1998. Effects of dietary vitamin E on the immune system in broilers: altered proportions of CD4 T cells in the thymus and spleen. Poultry Sci. 77:529.
  • Erf, G.F., and W.G. Bottje. 1996. Nutrition and immune function in chickens: benefits of dietary vitamin E supplementation. Proc. Ark. Nutri. Conf.
  • Forrest, V.J., et al., 1994. Oxidative stress-induced apoptosis prevented by Trolox. Free Radic. Biol. Med. 16:675.

 

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