Review Volume 4, Issue 8 pp 535—546
Sarcopenia, obesity, and natural killer cell immune senescence in aging: Altered cytokine levels as a common mechanism
- 1 Department of Pathology and Laboratory Medicine, Department of Microbiology, Immunology, and Molecular Genetics, and the Markey Cancer Center, University of Kentucky, Lexington, KY 40536, USA
- 2 Geriatric Research, Education, and Clinical Center, VA Puget Sound Health Care System, Seattle, WA 98108, Division of Gerontology and Geriatric Medicine, Department of Medicine, University of Washington, Seattle, WA 98195, and Seattle Institute for Biomedical and Clinical Research, Seattle, WA 98108, USA
received: June 6, 2012 ; accepted: August 28, 2012 ; published: August 29, 2012 ;https://doi.org/10.18632/aging.100482
How to Cite
Human aging is characterized by both physical and physiological frailty. A key feature of frailty, sarcopenia is the age-associated decline in skeletal muscle mass, strength, and endurance that characterize even the healthy elderly. Increases in adiposity, particularly in visceral adipose tissue, are almost universal in aging individuals and can contribute to sarcopenia and insulin resistance by increasing levels of inflammatory cytokines known collectively as adipokines. Aging also is associated with declines in adaptive and innate immunity, known as immune senescence, which are risk factors for cancer and all-cause mortality. The cytokine interleukin-15 (IL-15) is highly expressed in skeletal muscle tissue and declines in aging rodent models. IL-15 inhibits fat deposition and insulin resistance, is anabolic for skeletal muscle in certain situations, and is required for the development and survival of natural killer (NK) lymphocytes. We review the effect that adipokines and myokines have on NK cells, with special emphasis on IL-15. We posit that increased adipokine and decreased IL-15 levels during aging constitute a common mechanism for sarcopenia, obesity, and immune senescence.