Giant cell arteritis: immune and vascular aging as disease risk factors.

Giant cell arteritis: immune and vascular aging as disease risk factors.
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DOI:
10.1186/ar3358
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发表时间:
2011-08-02
影响因子:
4.9
通讯作者:
Weyand CM
Weyand CM
中科院分区:
医学2区
文献类型:
--
作者:
Mohan SV;Liao YJ;Kim JW;Goronzy JJ;Weyand CM

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巨细胞动脉炎的易感性随着年龄的增长而增加,与年龄相关的免疫系统重建和年龄诱导的血管壁重塑平行。免疫衰老导致幼稚T细胞池的缩小、T细胞多样性的收缩和先天免疫的损害。免疫活性细胞的老化迫使宿主采取保护性免疫的替代途径,并赋予致病性免疫的风险,导致慢性炎性组织损伤。随着衰老的宿主被迫科普不断增长的感染负荷,免疫能力的下降尤其相关。免疫衰老与血管老化同时发生,在此期间,动脉壁发生剧烈的结构变化,中型和大型动脉失去柔韧性和弹性。在分子水平上,弹性纤维退化,基质蛋白积累生化修饰。因此,衰老过程影响了两个主要的生物系统,这两个系统相互联系,促进巨细胞动脉炎;免疫系统和血管壁生态位。
Susceptibility for giant cell arteritis increases with chronological age, in parallel with age-related restructuring of the immune system and age-induced remodeling of the vascular wall. Immunosenescence results in shrinkage of the naïve T-cell pool, contraction of T-cell diversity, and impairment of innate immunity. Aging of immunocompetent cells forces the host to take alternative routes for protective immunity and confers risk for pathogenic immunity that causes chronic inflammatory tissue damage. Dwindling immunocompetence is particularly relevant as the aging host is forced to cope with an ever growing infectious load. Immunosenescence coincides with vascular aging during which the arterial wall undergoes dramatic structural changes and medium and large arteries lose their pliability and elasticity. On the molecular level, elastic fibers deteriorate and matrix proteins accumulate biochemical modifications. Thus, the aging process impacts the two major biologic systems that liaise to promote giant cell arteritis; the immune system and the vessel wall niche.
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