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Premature Immunosenescence in Rheumatoid Arthritis and Multiple Sclerosis Patients
Author(s) -
THEWISSEN MARIELLE,
LINSEN LOES,
SOMERS VEERLE,
GEUSENS PIET,
RAUS JEF,
STINISSEN PIET
Publication year - 2005
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1361.066
Subject(s) - immunosenescence , rheumatoid arthritis , medicine , immunology , immune system , premature aging , senescence , multiple sclerosis , autoimmune disease , peripheral blood mononuclear cell , autoimmunity , cd28 , thymic involution , t cell , antibody , biology , physiology , genetics , in vitro
A bstract : Patients with T‐cell‐mediated autoimmune diseases show immune system abnormalities that resemble the typical characteristics of autoimmune dysfunction described in the elderly. In addition, the incidence of autoimmune disease increases with advancing age. To evaluate whether patients with rheumatoid arthritis (RA) and multiple sclerosis (MS) have premature immuno‐senescence, we measured two indicators of aging: the number of T‐cell‐receptor excision circles (TRECs) and the percentage of CD4 + CD28 null T cells. We studied them in the peripheral blood mononuclear cells (PBMCs) of 60 RA patients, 32 MS patients, and 40 healthy controls (HCs). We found that TREC numbers were lower in RA and MS patients than in age‐matched HCs, indicating premature thymic involution. Moreover, a subset of these patients contained age‐inappropriate high frequencies of CD4 + CD28 null T cells. This study provides evidence of premature immune system senescence in both RA and MS patients. Premature aging could be a risk factor for developing autoimmune disorders in genetically predisposed individuals in a susceptible environment.