Source:http://linkedlifedata.com/resource/pubmed/id/12915205
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
2003-8-13
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pubmed:abstractText |
Current disease models of autoimmune syndromes, such as rheumatoid arthritis, propose that chronic inflammation is caused by 'forbidden T-cell clones' that recognize disease-inducing antigens and drive tissue-injurious immune reactions. Reappraisal of disease incidence data, however, emphasizes that rheumatoid arthritis is a syndrome of the elderly that occurs with highest likelihood in individuals in whom the processes of T-cell generation and T-cell repertoire formation are compromised. Thymic T-cell production declines rapidly with advancing age. Multiple mechanisms, including antigen-driven clonal expansion and homeostasis-driven autoproliferation of post-thymic T cells, impose replicative stress on T cells and induce the biological program of cellular senescence. T-cell immunosenescence is associated with profound changes in T-cell functional profile and leads to accumulation of CD4+ T cells that have lost CD28 but have gained killer immunoglobulin-like receptors and cytolytic capability and produce large amounts of interferon-gamma. In patients with rheumatoid arthritis, T-cell immunosenescence occurs prematurely, probably due to a deficiency in the ability to generate sufficient numbers of novel T cells. We propose that autoimmunity in rheumatoid arthritis is a consequence of immunodegeneration that is associated with age-inappropriate remodeling of the T-cell pool.
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pubmed:grant |
http://linkedlifedata.com/resource/pubmed/grant/R01 AG15043,
http://linkedlifedata.com/resource/pubmed/grant/R01 AI44142,
http://linkedlifedata.com/resource/pubmed/grant/R01 AR41974,
http://linkedlifedata.com/resource/pubmed/grant/R01 AR42527,
http://linkedlifedata.com/resource/pubmed/grant/R01 EY11916,
http://linkedlifedata.com/resource/pubmed/grant/R01 HL63919
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0531-5565
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
38
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
833-41
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:12915205-Adult,
pubmed-meshheading:12915205-Aged,
pubmed-meshheading:12915205-Aging,
pubmed-meshheading:12915205-Antigens, CD,
pubmed-meshheading:12915205-Arthritis, Rheumatoid,
pubmed-meshheading:12915205-Autoimmunity,
pubmed-meshheading:12915205-CD4-Positive T-Lymphocytes,
pubmed-meshheading:12915205-Cell Aging,
pubmed-meshheading:12915205-Coronary Artery Disease,
pubmed-meshheading:12915205-Humans,
pubmed-meshheading:12915205-Immune System,
pubmed-meshheading:12915205-Lymphocyte Count,
pubmed-meshheading:12915205-Middle Aged,
pubmed-meshheading:12915205-Thymus Gland
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pubmed:year |
2003
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pubmed:articleTitle |
Immunosenescence, autoimmunity, and rheumatoid arthritis.
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pubmed:affiliation |
Department of Medicine and Immunology, Mayo Clinic, Guggenheim 401, 200 First Street SW, Rochester, MN 55905, USA. weyand.cornelia@mayo.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Review,
Research Support, Non-U.S. Gov't
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