Origin of late-onset autoimmune disease

被引:16
|
作者
Hsu, HC
Mountz, JD
机构
[1] Univ Alabama, Dept Med, Div Clin Immunol & Rheumatol, Birmingham, AL 35294 USA
[2] Vet Adm Med Ctr, Birmingham, AL 35294 USA
关键词
T-CELL APOPTOSIS; ANTIGEN-PRESENTING CELLS; SYSTEMIC-LUPUS-ERYTHEMATOSUS; ALPHA-INDUCED APOPTOSIS; IN-VIVO; RHEUMATOID-ARTHRITIS; AGED MICE; REPLICATIVE SENESCENCE; PSORIATIC-ARTHRITIS; ELDERLY HUMANS;
D O I
10.1016/S0889-8561(02)00074-7
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Autoimmune disease in the elderly is hypothesized to be caused by an imbalance in T-cell expansion and deletion after all encounter with self-antigens. A decrease in thymic Output leads to a decreased pool of naive T cells in the periphery and to increased oligoclonal expansion of T cells. This expansion may be Caused by Stimulation with autoantigens that drive high-affinity interactions with self-antigens. Accumulation of presenescent, apoptosis-resistant, and proinflammatory T cells results in the growth of these autoreactive T cells. A decreased T-cell activation response that occurs with age leads to several defects that diminish the immune response.
引用
收藏
页码:65 / +
页数:21
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