Neuroendocrine and viral correlates of premature immunosenescence

May 7, 2015Annals of the New York Academy of Sciences

Links Between Hormone Systems, Viruses, and Early Aging of the Immune System

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Abstract

Chronic stress may accelerate immunosenescence in younger individuals, leading to shorter telomere lengths.

Chronic psychological stress is linked to features of immunosenescence, including thymic involution and decreased T cell proliferation.
Increased cortisol levels are connected to accelerated immunosenescence processes.
Human cytomegalovirus (CMV) infection could reduce the diversity of T cell receptors and promote the growth of senescent T cells.
Elevated inflammation, termed 'inflammaging,' is associated with age-related diseases and increased mortality.
Patients with rheumatoid arthritis demonstrate signs of premature immunosenescence, including the presence of senescent T cells and potential cognitive decline.
Bipolar disorder may serve as a model for accelerated aging due to associations with shortened telomeres and increased senescent T cells.

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Aging continuously remodels the immune system, a process known as immunosenescence. Here, we review evidence of premature immunosenescence in younger individuals under conditions of chronic psychological stress, chronic inflammation, or exposure to certain persistent viral infections. Chronic stress may accelerate various features of immunosenescence by activating key allostatic systems, notably the hypothalamic-pituitary-adrenal axis and increased cortisol levels. Chronic stress is associated with thymic involution, blunted T cell proliferation, increased serum proinflammatory markers, and shorter telomere lengths. Human cytomegalovirus (CMV) infection has been implicated in accelerating immunosenescence by shrinking the T cell receptor repertoire and causing clonal expansion of senescent CD8(+) CD28(-) T cells with a proinflammatory profile. These factors increase inflammation associated with aging, or "inflammaging," particularly as it relates to etiology of several age-related diseases and increased mortality. Patients with rheumatoid arthritis have been shown to have several signatures of premature immunosenescence, including expansion of senescent T cells associated with cognitive impairment. We end by speculating that bipolar disorder can be considered as a model of accelerated aging because it has been associated with shortened telomeres, higher CMV IgG titers, and expansion of senescent and regulatory T cells.

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Neuroendocrine and viral correlates of premature immunosenescence

Abstract

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