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Posted on Jun 14, 2006, 2 p.m.
By Bill Freeman
Aging is associated with a paradox of immunodeficiency and inflammation (an evidence of hyperactive immune system). Apoptosis is associated with cellular depletion and suppression of inflammatory response. In this brief review, we will present evidence for the role of increased apoptosis in immunodeficiency and paradoxical increased inflammation associated with human aging.
Aging is associated with a paradox of immunodeficiency and inflammation (an evidence of hyperactive immune system). Apoptosis is associated with cellular depletion and suppression of inflammatory response. In this brief review, we will present evidence for the role of increased apoptosis in immunodeficiency and paradoxical increased inflammation associated with human aging. In particular, a role of apoptotic cells in failure to generate anti-inflammatory responses and directly activating inflammatory responses will be discussed.
Aging represents a paradox of immune deficiency and chronic inflammation. Immune deficiency is predominantly associated with progressive decline in T cell functions in both mice and humans and numbers in humans, whereas, chronic inflammation is evidenced by increased circulating levels of pro-inflammatory cytokines, (IL-6, TNF-α, IL-1β,), acute phase proteins including C-reactive protein and serum amyloid A, and increased frequency of chronic inflammatory diseases of aging such as Alzheimer's Parkinson's diseases, amyotrophic lateral sclerosis, atherosclerosis etc.
