Page 1387 - Veterinary Immunology, 10th Edition
P. 1387

Some vitamins, most notably A, D, and E, play a key role in
  VetBooks.ir  regulating immunity.

                  Vitamin A metabolites, especially retinoic acid, enhance
               cytotoxicity and T cell proliferation by stimulating IL-2 production.

               Conversely, vitamin A deficient mice have defective helper T cell
               activity. Retinoic acid can inhibit B cell proliferation and inhibit B
               cell apoptosis. Retinoic acid also enhances dendritic cell antigen
               presentation and maturation. Vitamin A metabolites can modulate

               the Th1-Th2 balance as well as the differentiation of Treg and Th17
               cells (Chapter 21). Retinoic acid also regulates the gut-homing
               abilities of T and B cells, and a vitamin A deficiency is associated
               with impaired gastrointestinal immune responses and increased

               susceptibility to gastrointestinal and respiratory diseases (Chapter
               40). If a pregnant mouse lacks vitamin A, her offspring have small
               lymph nodes and have an impaired immune response as adults.
                  Vitamin D, as described previously (Chapter 40), also plays a key

               role in immunity. The most important form, vitamin D , is
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               synthesized within the skin or the liver, kidneys, and lymphoid
               tissues. Macrophages and dendritic cells require vitamin D for the

               production of the antimicrobial peptide cathelicidin. The vitamin D
               receptor is upregulated by IL-15 triggered by T cell receptor (TCR)
               activation.

                  Vitamin E and selenium affect immune responses and disease
               resistance in poultry, pigs, and laboratory animals. A deficiency of
               vitamin E ([dl]-α-tocopheryl-acetate) results in immunosuppression
               and reduced resistance to disease. On the other hand,
               supplementation of diets with vitamin E can enhance certain

               immune responses. Lymphocyte responses to pokeweed mitogen
               are higher in pigs with high vitamin E levels. Vitamin E
               supplementation given to cows for several weeks before calving

               prevents the decline in neutrophil function and macrophage
               function that normally occurs in the immediate post-parturient
               period. Vitamin E promotes B cell proliferation; the effect is most
               marked in the primary immune response. It can act as an adjuvant
               when administered with Brucella ovis vaccine, clostridial toxoid, and

               Escherichia coli J5 vaccine. In some cases, this increased antibody
               production may lead to increased disease resistance. Vitamin E can
               reduce age-related declines in immune function by a direct action





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