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Beta-Amyloid Peptides Enhance the Proliferative Response of Activated CD4.sup.+CD28.sup.+ Lymphocytes from Alzheimer Disease Patients and from Healthy Elderly

Alzheimer's disease (AD) is the most frequent form of dementia among elderly. Despite the vast amount of literature on non-specific immune mechanisms in AD there is still little information about the potential antigen-specific immune response in this pathology. It is known that early stages of...

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Bibliographic Details
Published in:PloS one 2012-03, Vol.7 (3), p.e33276
Main Authors: Józwik, Agnieszka, Landowski, Jerzy, Bidzan, Leszek, Fülop, Tamas, Bryl, Ewa, Witkowski, Jacek M
Format: Article
Language:English
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Summary:Alzheimer's disease (AD) is the most frequent form of dementia among elderly. Despite the vast amount of literature on non-specific immune mechanisms in AD there is still little information about the potential antigen-specific immune response in this pathology. It is known that early stages of AD include [beta]-amyloid (A[beta])- reactive antibodies production and inflammatory response. Despite some evidence gathered proving cellular immune response background in AD pathology, the specific reactions of CD4.sup.+ and CD8.sup.+ cells remain unknown as the previous investigations yielded conflicting results. Here we investigated the CD4.sup.+ CD28.sup.+ population of human peripheral blood T cells and showed that soluble [beta]-amyloids alone were unable to stimulate these cells to proliferate significantly, resulting only in minor, probably antigen-specific, proliferative response. On the other hand, the exposure of in vitro pre-stimulated lymphocytes to soluble A[beta] peptides significantly enhanced the proliferative response of these cells which had also lead to increased levels of TNF, IL-10 and IL-6. We also proved that A[beta] peptide-enhanced proliferative response of CD4.sup.+ CD28.sup.+ cells is autonomous and independent from disease status while being associated with the initial, ex vivo activation status of the CD4.sup.+ cells. In conclusion, we suggest that the effect of A[beta] peptides on the immune system of AD patients does not depend on the specific reactivity to A[beta] epitope(s), but is rather a consequence of an unspecific modulation of the cell cycle dynamics and cytokine production by T cells, occurring simultaneously in a huge proportion of A[beta] peptide-exposed T lymphocytes and affecting the immune system performance.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0033276