Women with the Alzheimer's risk marker ApoE4 lose Aβ-specific CD4⁺ T cells 10-20 years before men.

ABSTRACT: Adaptive immunity to self-antigens causes autoimmune disorders, such as multiple sclerosis, psoriasis and type 1 diabetes; paradoxically, T- and B-cell responses to amyloid-β (Aβ) reduce Alzheimer's disease (AD)-associated pathology and cognitive impairment in mouse models of the disease. The manipulation of adaptive immunity has been a promising therapeutic approach for the treatment of AD, although vaccine and anti-Aβ antibody approaches have proven difficult in patients, thus far. CD4(+) T cells have a central role in regulating adaptive immune responses to antigens, and Aβ-specific CD4(+) T cells have been shown to reduce AD pathology in mouse models. As these cells may facilitate endogenous mechanisms that counter AD, an evaluation of their abundance before and during AD could provide

SUBMITTER: Begum AN 

PROVIDER: S-EPMC4119219 | biostudies-literature | 2014 Jul

REPOSITORIES: biostudies-literature