Aβ1–42 stimulated T cells express P-PKC-δ and P-PKC-ζ in Alzheimer disease
Autor: | Alessandro Di Siena, Eugenio Santavenere, Domenico Gambi, Adriana Bascelli, Marco Marchisio, Sebastiano Miscia, Philip M. Grimley, Laura Pierdomenico, Francesco Gambi, Fausta Ciccocioppo, Giampiero Ausili-Cèfaro, Domenico Genovesi, Paola Lanuti, Lucia Velluto |
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Rok vydání: | 2009 |
Předmět: |
Regulation of gene expression
Aging medicine.medical_specialty biology Amyloid beta business.industry General Neuroscience CD3 CD28 T lymphocyte medicine.disease Endocrinology Internal medicine biology.protein medicine Neurology (clinical) Geriatrics and Gerontology Signal transduction Alzheimer's disease business Protein kinase C Developmental Biology |
Zdroj: | Neurobiology of Aging. 30:394-406 |
ISSN: | 0197-4580 |
Popis: | The protein kinase C (PKC) family of enzymes is a regulator of transmembrane signal transduction, and involvement of some PKC isoforms in T-cell activation has been demonstrated. Nevertheless, very little is known about their involvement in the Amyloid beta (Abeta)-dependent molecular signals in the T lymphocytes of Alzheimer disease (AD) patients. Therefore, the aim of this study was to investigate the involvement of PKC-alpha, PKC-delta and PKC-zeta expression and activity in the signaling machinery activated in Abeta-reactive T cells, in adult healthy individuals, elderly healthy subjects, and from patients with AD. The results show that in peripheral T-cells from early AD patients, Abeta(1-42) produced a distinct subpopulation highly expressing P-PKC-delta, while in severe AD patients the same treatment induced two distinct P-PKC-delta and P-PKC-zeta T-cell subpopulations. Such subpopulations were not noticeable following CD3/CD28 treatment of the same samples or after treatment of peripheral T cells from healthy adult or elderly subjects with Abeta(1-42) or with CD3/CD28. We believe that these findings may be of help in possible attempts to develop further diagnostic strategies useful for the characterization of AD. |
Databáze: | OpenAIRE |
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