Page 1353 - Veterinary Immunology, 10th Edition
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                             FIG. 40.8  The effects of a vitamin A deficiency on the immune
                                                         system.


                  A prenatal vitamin A deficiency affects the responses of piglets to

               rotavirus vaccine. Deficient piglets shed the virus at 350% of the
               level of vitamin A sufficient piglets. Only 25% of the deficient
               piglets were protected as compared to 100% of the sufficient piglets.
               Deficient piglets had fewer IgG secreting cells in the ileum and
               fewer IgA secreting cells in the duodenum. Intestinal IgA titers

               were 11-fold less than in vitamin A sufficient animals. Deficient
               animals did, however, have higher levels of IL-8 and IFN-γ than
               sufficient piglets.

                  Calves fed a low vitamin A diet and immunized with an
               inactivated bovine coronavirus vaccine had reduced IgG1 antibody
               levels against bovine coronavirus, suggesting that Th2 responses
               may be impaired in these animals.
                  Vitamin E is a major antioxidant in cell membranes and is

               important in regulating the oxidants produced by phagocytic cells.
               Vitamin E deficiency depresses immunoglobulin levels through its
               effects on Treg cells and decreases lymphocyte responses to

               mitogens. Animals deficient in vitamin E also show reduced IL-2
               and transferrin receptor expression and depressed phagocytic
               function. Vitamin E is one of the few vitamins for which
               supplementation has been shown to enhance immune responses
               and disease resistance. The importance of vitamin E for proper

               functioning of the immune system has been seen in an inbred
               population of donkeys whose foals were dying from overwhelming
               bacterial infections at 3 to 5 months of age. Investigations revealed





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