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

Abstract：

: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.

journal_name

Arthritis Res Ther

journal_title

Arthritis research & therapy

authors

Mohan SV,Liao YJ,Kim JW,Goronzy JJ,Weyand CM

doi

10.1186/ar3358

subject

Has Abstract

pub_date

2011-08-02 00:00:00

pages

231

issue

4

eissn

1478-6354

issn

1478-6362

pii

ar3358

journal_volume

13

pub_type

杂志文章,评审

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