T cell response to amyloid-β and to mitochondrial antigens in Alzheimer's disease

被引:25
|
作者
Giubilei, F [1 ]
Antonini, G [1 ]
Montesperelli, C [1 ]
Sepe-Monti, M [1 ]
Cannoni, S [1 ]
Pichi, A [1 ]
Tisei, P [1 ]
Casini, AR [1 ]
Buttinelli, C [1 ]
Prencipe, M [1 ]
Salvetti, M [1 ]
Ristori, G [1 ]
机构
[1] Univ Roma La Sapienza, Dipartimento Sci Neurol, I-00185 Rome, Italy
关键词
Alzheimer's disease; amyloid-beta; T lymphocytes; T cell reactivity; mitochondrial antigens;
D O I
10.1159/000069991
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Despite the vast amount of literature on non-specific immune mechanisms in Alzheimer's disease (AD), little is known about the role of antigen-specific immune responses. We investigated T cell reactivity to fragment 1-42 of amyloid-beta (Abeta) and to N-terminal peptides of human mitochondrial and control microbial proteins. Thirty subjects with a diagnosis of probable AD according to NINCDS-ADRDA criteria and 30 sex- and age-matched healthy controls were enrolled. T cell responses to Abeta fragment showed no significant differences between AD patients and controls. By contrast, the mean number of positive T cell responses to both human mitochondrial and microbial peptides was significantly decreased in AD patients compared to control subjects. No significant correlation was found between T cell responses and both the severity of cognitive impairment and duration of the disease. Our results suggest that antigen-specific immune responses are impaired in AD. Protective immune responses to harmful amyloidogenic substances may also be impaired, thus favoring their accumulation in the brain. Copyright (C) 2003 S. Karger AG, Basel.
引用
收藏
页码:35 / 38
页数:4
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