Abstract
There is substantial evidence to support
an important role for zinc in immune processes. Adequate zinc status is
essential
for T-cell division, maturation and
differentiation; lymphocyte response to mitogens; programmed cell death
of lymphoid and
myeloid origins; gene transcription; and
biomembrane function. Lymphocytes are one of the types of cells
activated by zinc.
Zinc is the structural component of a wide variety
of proteins, neuropeptides, hormone receptors and polynucleotides. Among
the best known zinc-dependent hormones/enzymes are
Cu, Zn superoxide dismutase, an enzyme component of the antioxidant
defense
system, and thymulin, which is essential for the
formation of T-lymphocytes. In animals and humans, zinc deficiency
results
in rapid and marked atrophy of the thymus, impaired
cell-mediated cutaneous sensitivity and lymphopenia. Primary and
secondary
antibody responses are reduced in zinc deficiency,
particularly for those antigens that require T-cell help, such as those
in heterologous red blood cells. In addition,
antibody response and the generation of splenic cytotoxic T cells after
immunization
are reduced. Zinc also inhibits the production of
tumor necrosis factor, which is implicated in the pathophysiology of
cachexia
and wasting in acquired immune deficiency syndrome.
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