Rheumatoid Arthritis: A Role for Immunosenescence?

Aging is accompanied by a progressive decline in the integrity of the immune system, a process known as immunosenescence. Pathological features typical of immune dysfunction in older adults, encompassing dysregulation of innate and adaptive immune responses, characterize rheumatoid arthritis (RA), a...

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Bibliographic Details
Published in:Journal of the American Geriatrics Society (JAGS) 2010-08, Vol.58 (8), p.1565-1575
Main Authors: Lindstrom, Tamsin M., Robinson, William H.
Format: Article
Language:English
Subjects:
Adaptive Immunity - physiology
Aging
Aging - immunology
Antigens, Differentiation, T-Lymphocyte - physiology
Arthritis, Rheumatoid - immunology
autoimmunity
Autoimmunity - physiology
B-Lymphocytes - physiology
CD28
CD4-Positive T-Lymphocytes - physiology
Cell Proliferation
Cytokines - physiology
Dendritic Cells - physiology
Humans
Immune system
Immune System - physiology
immunosenescence
Leukocyte Count
Pathology
Rheumatoid arthritis
T-Lymphocytes - physiology
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Summary:Aging is accompanied by a progressive decline in the integrity of the immune system, a process known as immunosenescence. Pathological features typical of immune dysfunction in older adults, encompassing dysregulation of innate and adaptive immune responses, characterize rheumatoid arthritis (RA), an autoimmune disease whose incidence increases with age. Recent evidence suggests that certain features of immunosenescence, such as the decrease in T‐cell generation and diversity, may contribute to the development of RA. Thus, physiological immunosenescence may render older adults susceptible to RA, and premature immunosenescence may contribute to the development of RA in young adults. In addition, other features of immunosenescence may result from the chronic immune stimulation that occurs in RA and lead to worsening of the disease. This article reviews the immunopathological features common to aging and RA and discusses the mechanisms by which immunosenescence may contribute to the development or progression of RA.
ISSN:0002-8614
1532-5415
DOI:10.1111/j.1532-5415.2010.02965.x