Inflamm-aging: autoimmunity, and the immune-risk phenotype

被引:163
作者
Boren, E [1 ]
Gershwin, ME [1 ]
机构
[1] Univ Calif Davis, Sch Med, Dept Internal Med, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA
关键词
immunosenescence; autoimmunity; immune-risk phenotype;
D O I
10.1016/j.autrev.2004.03.004
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Aging of the immune system, or immunosenescence, is a complex subject best defined as a decline in cell-mediated immunity, particularly with respect to T cell function. Paradoxically with the decline in immune function is an increase in autoantibody frequency. It has been postulated that the accumulation of anamnestic cells over time and/or environmental/ infectious mimics leads to the production of autoantibodies, sometimes accompanied by autoimmune disease. This specific phenotype has given rise to the concept of a specific cluster of cytokine profiles, coined an immune-risk phenotype (IRP). The IRP is likely dictated by not only cytokine production, but also defects in activation-induced cell death and also a shift in T cell subsets. These concepts are an important bridge between basic immune function and clinical immunology in the hopes for generation of effective reconstitution to improve immune function in the elderly. (C) 2004 Elsevier B.V. All rights reserved.
引用
收藏
页码:401 / 406
页数:6
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