The formation of new red and white blood cells and platelets is one of the most proliferation-dependent physiological processes of the body. The various classes of circulating white cells are the underpinning of the host defense system, together with tissue macrophages, hepatic proteins, and the alimentary tract's mucosa.
Hematological aging The blood-forming organ is the bone marrow. Aging is associated with fatty infiltration of the marrow spaces in the long bones, but enough marrow remains to support the turnover of erythrocytes and red blood cell lines. The circulating red blood cell mass does not normally change with advancing age, nor does the normative peripheral white cell count or platelet number. As noted, iron stores tend to be abundant in later life; nutritional problems influencing red blood cell production are based on alterations in gastric function (vitamin B12 malabsorption), which result in a macrocytic (megaloblastic) anemia.
Immunological aging Circulating phagocytic white blood cells counts do not reduce with aging but aging does influence the innate host defense system. Mucosal barrier functions are influenced by aging of the gut in its interaction with microflora. Although not reduced in number, aged macrophages and neu-trophils have blunted intracellular signaling by specific receptors, decreased metabolic functions, and impaired bacterial killing. Production of superoxide anion, chemotaxis, and orderly apoptosis of neutro-phils is also disrupted by the disordered signaling. The tumor cell-destroying capacity of natural killer (NK) cells in the elderly is diminished.
More profound changes occur in the adaptive immune functions, which rely on the memory (T cell) lymphocytic cell line. Life-long antigen exposure induces increases in the number of memory T cells, but with enhanced reactivity against self-antigens, priming the individual for autoimmune disease. In healthy adults, IgA concentration increases by 0.2 gl"1 per decade throughout life. The T lymphocytes, however, respond more poorly to ongoing antigen assault in later life. Thymic involution associated with neural and hormonal changes of aging is an impediment to T-cell maturation in older persons. The basis of intrinsic function deficits of memory cells, on the other hand, has been ascribed to defective signaling and includes hyporesponsive-ness to mitogen-stimulated proliferation and decrease in genetic suppression, allowing increased stimulation of inflammatory cytokines; the balance between pro-and anti-inflammatory cytokines shifts with aging, favoring the inflammatory pole, especially with the greater expression of interleukin 6. This has a negative systemic effect on bone metabolism, as well as dysregulating overall immune function.
Aging of mitochondria in the immune cell lines produces increased intracellular reactive oxygen species burdens. Finally, there is diminished programed death (apoptosis) of immune cells and dysregulation of apoptosis-dependent functions.
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