Inflamm-aging: autoimmunity, and the immune-risk phenotype
Inflamm-aging: autoimmunity, and the immune-risk phenotype
复制标题
DOI：
10.1016/j.autrev.2004.03.004
复制
发表时间：
2004-07-01
影响因子：
13.6
通讯作者：
Gershwin, ME
中科院分区：
文献类型：
--
作者：
Boren, E;Gershwin, ME
免疫系统的老化或免疫衰老是一个复杂的主题，最好定义为细胞介导的免疫力下降，特别是关于T细胞功能。特别是随着免疫功能的下降，自身抗体频率增加。据推测，记忆细胞随时间和/或环境/感染模拟物的积累导致自身抗体的产生，有时伴有自身免疫性疾病。这种特定的表型引起了细胞因子谱的特定簇的概念，创造了免疫风险表型（IRP）。IRP可能不仅由细胞因子产生决定，而且还由活化诱导的细胞死亡的缺陷以及T细胞亚群的转变决定。这些概念是基础免疫功能和临床免疫学之间的重要桥梁，希望产生有效的重建，以提高老年人的免疫功能。(C)2004 Elsevier B. V.保留所有权利。
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.