Aging and the skin immune system.
OBJECTIVE
To give a brief summary of age-related alterations that occur in the immune system (immunosenescence), with special regard to the skin immune system.


METHODS
MEDLINE and institutional libraries were searched for relevant articles on immunosenescence and corresponding key words.


RESULTS
The immune system of aged animals and humans undergoes alterations that may account for an increased susceptibility to certain infections, autoimmune diseases, or malignancies. However, some data on the parameters of immunosenescence are controversial. This appears to be caused by variations in study designs or by the many external influences that superimpose on intrinsic alterations of the immune system. Well characterized are age-related changes of T cells and cell-mediated immunity. With advancing age, human and murine T cells undergo a shift from the naive to the memory phenotype, associated with a change in cytokine profile. The cells also reveal reductions in the proliferative response to activation, in diversity of the T-cell receptor antigen repertoire, and in cytolytic activity. B cells of aging individuals show a restricted diversity of their antibody repertoire due to a decline in somatic mutations, resulting in a reduced response to certain viral infections or vaccinations. The number of Langerhans cells appears to decline with age, contributing to a reduced rate of sensitizations. Macrophages and keratinocytes also undergo age-related changes, although these are less well characterized. They entail alterations in cytokine production, which could play a role in increased susceptibility to endotoxins in elderly individuals.


CONCLUSIONS
With aging, the skin immune system shows a decline in its adaptive capability, one of its outstanding qualities. Manipulations to revert age-related dysfunctions are being tested and may help to extend a healthy life.
Sunderkötter
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Department of Dermatology, Ludwig Boltzmann Institute of Cellbiology and Immunobiology of the Skin, University of Münster, Germany.
Kalden
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Luger
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TA
D000222:Adaptation, Physiological / Q000276:immunology; D000368:Aged; D000375:Aging / Q000276:immunology*; D000818:Animals; D000906:Antibodies / Q000276:immunology; D001327:Autoimmune Diseases / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology; D001424:Bacterial Infections / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D004198:Disease Susceptibility / Q000276:immunology; D004731:Endotoxins / Q000276:immunology; D006801:Humans; D007111:Immunity, Cellular / Q000276:immunology; D007156:Immunologic Memory; D016130:Immunophenotyping; D015603:Keratinocytes / Q000276:immunology; D007801:Langerhans Cells / Q000276:immunology; D008213:Lymphocyte Activation / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D051379:Mice; D009154:Mutation / Q000276:immunology; D009369:Neoplasms / Q000276:immunology; D011948:Receptors, Antigen, T-Cell / Q000276:immunology; D012867:Skin / Q000276:immunology*; D012879:Skin Physiological Phenomena; D013601:T-Lymphocytes / Q000276:immunology; D014611:Vaccination; D014777:Virus Diseases / Q000276:immunology
D000906:Antibodies; D016207:Cytokines; D004731:Endotoxins; D011948:Receptors, Antigen, T-Cell