Aging and the Immune System
An article by A. J. Lanigan
Immunosenescence: Age-associated immune deficiency
Biological aging is the consequence of time on an individual. In general terms, a person passes through two periods in life. Development occurs early in life, when biological function increases and becomes more adaptive. This is followed by sensescence[1], when biological function decreases and becomes less adaptive. During senescence, physiological variance increases as homeostatic reserve diminishes.
Immune senescence is associated with a greater frequency of infectious and neoplastic diseases. Research has revealed that in the USA infectious disease ranks 8th among most causes of death but rises to rank fourth in persons over 65. Similarly, cancer incidence increases exponentially after the age of 30.
Immune senescence and the decline in "immune surveillance" at least contribute to these statistical increases. Major shifts in certain immunological markers usually precede the appearance of leukemia, multiple myeloma, and lymphoma.
Immune senescence is more precisely characterized by shifts in the number, distribution, and activity of lymphocyte subsets, antibody specificities, and cytokines with age. For this reason, immune senescence is best described as a process leading to immune dysregulation.
Dysregulation occurs in the cell-mediated and the humoral immune systems. Two very important areas stand out. One is cytokine production and the other is the shift in B cell production of autoantibodies.
Evidence for immune senescence of T cells[2]:
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Gradual loss of production of naive T cells with compensatory increase in memory T cells1.
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The shrinking of size and function of the thymus.
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Loss of Delayed Type hypersensitivity (DTH).
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Evidence of a Th1 to a Th2 cytokine switch.
Evidence for immune senescence in B cells[3]:
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Increase in B cell death due to lack of proper gene rearrangement.
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Impaired production of naive B cells in bone marrow.
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Skewing of production of B cells that product autoantibodies.
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Loss of new antibody production.
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Increase in Ig production (monoclonal and oligoclonal)
Beta Glucan affects macrophages, neutrophils, and natural killer cells in a manner that is well understood. Activities involving these glucan responsive cells could impact outcome or, delay the outcome of most items listed due to aging of the immune system. Should not this be part of your anti-aging scheme?
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- The state between maturity and death.
- http://www.csa.com/discoveryguides/archives/immune-aging.php
- http://www.health.harvard.edu/flu-resource-center/how-to-boost-your-immune-system.htm
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