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vitamin B and immunity 744 vitronectin
to atrophy of thymus, spleen, lymph nodes, and Peyer’s
patches, pointing to major alterations of immune effector
cell mechanisms. Vitamin A deficiency is also associated
with impaired ability to form antibody responses to
T cell-dependent antigens such as tetanus toxoid, proteins,
and viral infections. It is also linked to decreased antibody
responsiveness to T cell-independent antigens such
as pneumococcal and meningococcal polysaccharides.
Vitamin A deficiency also compromises natural innate
immunity because it is necessary for maintenance of
mucosal surfaces, the first line of defense against infection.
Immune effector cells that mediate nonspecific immunity
include polymorphonuclear cells, macrophages, and natural
killer (NK) cells. Neutrophil phagocytosis is diminished by
vitamin A deficiency, and viral infections are more severe
because of diminished cytolytic activity by NK cells.
vitamin B and immunity
B complex vitamins differ greatly in chemical structures
and biological actions. Vitamin B 6 deficiency induces
marked changes in immune function, especially in the
thymus. Thymic hormone activity is diminished and
lymphopenia occurs. Vitamin B 6 deficiency suppresses
delayed cutaneous hypersensitivity responses, primary
and secondary T cell mediator cytotoxicity, and skin graft
rejection. It also impairs humoral immunity and the number
of circulating lymphocytes is decreased. Folate and vitamin
B 12 deficiencies are linked to diminished host resistance
and impaired lymphocyte function. Pantothenic acid deficiency
suppresses humoral antibody responses to antigens.
Thiamin, biotin, and riboflavin deficiencies induce moderate
interference with immune function. Riboflavin deficiency
diminishes humoral antibody formation in response
to antigen. Intake of micronutrients, including B complex
vitamins at doses two to three times higher than the U.S.
recommended daily allowance (RDA) help maintain optimal
immune function in healthy elderly adults.
vitamin C and immunity
Ascorbic acid (vitamin C) is necessary for proper functioning
of cells, tissues, and organs. It is an antioxidant and
a cofactor in many hydroxylating reactions. The immune
system is sensitive to levels of vitamin C intake. Leukocytes
have high concentrations of ascorbate that are used rapidly
during infection and phagocytosis, indicating the role of
vitamin C in immunity. Vitamin C facilitates neutrophil
chemotaxis and migration, induces interferon synthesis,
maintains mucus membrane integrity, and plays a role in
the expression of delayed-type hypersensitivity. High-dose
vitamin C supplementation is believed to increase T and
B lymphocyte proliferation. It diminishes nonspecific
extracellular free radical injury and autotoxicity after the
oxidative burst activity of stimulated neutrophils. It further
enhances immune function indirectly by maintaining optimal
levels of vitamin E.
vitamin D and immunity
Calcitriol, the hormonal form of vitamin D, plays a significant
regulatory role in cell differentiation and proliferation
of the immune system. It mediates its action through specific
intracellular vitamin D 3 receptors (VDRs). Among the
numerous effects of calcitriol on the immune system are the
inhibition of cytokine release from monocytes, prolongation
of skin allograft survival in mice, inhibition of autoimmune
encephalomyelitis and thyroiditis in mice, potentiation of
murine primary immune responses, restoration of defective
macrophage and lymphocyte functions in vitamin
D-deficient patients with rickets, restoration of lymphocyte
proliferation, and interleukin-2 (IL2) synthesis in human
dialysis patients, among many others.
vitamin E and immunity
Vitamin E is required by the immune system. It is a
major antioxidant that protects cell membranes from free
radical attack and is effective in preventing biological
injury by immunoenhancement. Vitamin E in high doses
diminishes CD8 + T cells and increases the CD4 + to CD8 +
T cell ratio; increases total lymphocyte count; and stimulates
cytotoxic natural killer (NK) cells, phagocytosis by
macrophages, and mitogen responsiveness. Its immunostimulatory
action renders it useful for therapeutic
enhancement of immune responses. The effect of vitamin
E on the immune system depends on its interaction with
other antioxidant and preoxidant nutrients, polyunsaturated
fatty acids, and other factors that affect immune
response, including age and stress. Vitamin E stimulation
of immunity is particularly important in the elderly
because infectious disease and tumor incidence increase
with age. Vitamin E facilitates host defense by inhibiting
increases in tissue prostaglandin synthesis from arachidonic
acid during infection. In vitro, vitamin E has been
shown to stimulate interleukin-2 (IL2) and interferon γ
(IFN-γ) by mitogen-stimulated lymphocytes. Vitamin
E prevents lipid peroxidation of cell membranes which
may be a mechanism to enhance immune responses and
phagocytosis.
vitiligo
Loss of skin or hair pigmentation as a consequence of
autoantibodies against melanocytes. The Smyth chicken is a
partially inbred line that exhibits a post-hatching depigmentation
of feathers as a consequence of an autoimmune
process; 95% of the depigmented chicks have detectable
autoantibodies several weeks prior to the appearance of
depigmentation. The autoantigen is a tyrosinase-related
protein. Smyth chicken amelanosis and human vitiligo are
similar in that their onset is in early adulthood and is often
associated with other autoimmune diseases, especially
those of the thyroid gland. Vitiligo may also result from a
polygenic disorder or sporadically. It is a syndrome marked
by acquired loss of pigmentation in a usually symmetrical
but spotty distribution, usually involving the central face
and lips, genitalia, hands, and extremities. Skin pigmentation
is produced by melanin, which is present in melanosomes
that are transferred to keratinocytes to protect
the skin against light. The two stages in the production
of vitiligo may be sequential. Type I vitiligo is marked
by decreased melanocyte tyrosinase activity, and type II
vitiligo is characterized by destruction of melanocytes.
Melanocytes and keratinocytes in the borders of vitiligo
lesions exhibit increased intercellular adhesion molecule 1
(ICAM-1) expression.
vitronectin
A 65-kDA cell adhesion glycoprotein found in serum at a
concentration of 20 mg/L. It combines with coagulation and
fibrinolytic proteins and with C5b67 complex to block its
insertion into lipid membranes. Vitronectin appears in basement
membranes along with fibronectin in proliferative vitreoretinopathy.
It decreases nonselective lysis of autologous