Aβ1–42 stimulated T cells express P-PKC-δ and P-PKC-ζ in Alzheimer disease

Miscia, Sebastianó; Ciccocioppo, Fausta; Lanuti, Paola; Velluto, Lucia; Bascelli, Adriana; Pierdomenico, Laura; Genovesi, Domenico; Siena, A. Di; Santavenere, Eugenio; Gambi, Francesco; Ausili-Cefaro, G; Grimley, Philip M.; Marchisio, Marco; Gambi, D.

doi:10.1016/j.neurobiolaging.2007.07.011

Cited by 39 publications

(30 citation statements)

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“…activated T cells, not Tregs) in AD patients compared to old controls. These data are in agreement with others reporting a higher frequency of activated cells in the PBMC of AD patients (Pellicanò et al, 2010;Monsonego et al, 2003;Miscia et al, 2009;Ciccocioppo et al, 2008), but seem discordant with a recent report on increased levels of Tregs in AD (Saresella et al, 2010). The presence of activated CD4+ T cells might be the result of Aβ-specific chronic T cell stimulation, creating a pro-inflammatory environment, and enhancing disease progression.…”

Section: Discussionsupporting

confidence: 84%

Immune profiling of Alzheimer patients

Pellicanò

Larbi

Goldeck

et al. 2012

Journal of Neuroimmunology

132

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Alzheimer's disease (AD) is characterized by extracellular senile plaques in the brain, containing amyloid-β peptide (Aβ). We identify immunological differences between AD patients and age-matched controls greater than those related to age itself. The biggest differences were in the CD4+ rather than the CD8+ T cell compartment resulting in lower proportions of naïve cells, more late-differentiated cells and higher percentages of activated CD4+CD25+ T cells without a Treg phenotype in AD patients. Changes to CD4+ cells might be the result of chronic stimulation by Aβ present in the blood. These findings have implications for diagnosis and understanding the aetiology of the disease.

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