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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