49 Citazioni (Scopus)

Abstract

To investigate the systemic signs of immune-inflammatory responses in Alzheimer’s disease (AD), in the present studywe have analyzed blood lymphocyte subsets and the expression of activation markers on peripheral blood mononuclear cells(PBMCs) fromADpatients and age-matched healthy controls (HC) activated in vitro by recombinant amyloid-β peptide (rAβ42).Our study of AD lymphocyte subpopulations confirms the already described decrease of the absolute number and percentage ofB cells when compared to HC lymphocytes, whereas the other subsets are not significantly different in patients and controls.We report the increased expression of the activation marker CD69 and of the chemokine receptors CCR2 and CCR5 on T cellsbut no changes of CD25 after activation. B cells are also activated by rAβ42 as demonstrated by the enhanced expression ofCCR5. Moreover, rAβ42 induces an increased expression of the scavenger receptor CD36 on monocytes. Some activationmarkers and chemokine receptors are overexpressed in unstimulated AD cells when compared to controls. This is evidence ofthe pro-inflammatory status of AD. Stimulation by rAβ42 also induces the production of the pro-inflammatory cytokines IL-1β,IL-6, IFN-γ, and TNF-α, and of the anti-inflammatory cytokines IL-10 and IL-1Ra. The chemokines RANTES, MIP-1β, andeotaxin as well as some growth factors (GM-CSF, G-CSF) are also overproduced by AD-derived PBMC activated by rAβ42.These results support the involvement of systemic immunity in AD patients. However, our study is an observational one so wecannot draw a conclusion about its contribution to the pathophysiology of the disease.
Lingua originaleEnglish
pagine (da-a)181-192
Numero di pagine12
RivistaJournal of Alzheimer's Disease
Volume21
Stato di pubblicazionePublished - 2010

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Alzheimer Disease
Cytokines
Chemokine Receptors
Lymphocyte Subsets
Blood Cells
Interleukin 1 Receptor Antagonist Protein
Scavenger Receptors
Chemokine CCL5
Granulocyte Colony-Stimulating Factor
Granulocyte-Macrophage Colony-Stimulating Factor
Interleukin-1
Chemokines
Amyloid
Interleukin-10
Observational Studies
In Vitro Techniques
Monocytes
Immunity
Interleukin-6
Intercellular Signaling Peptides and Proteins

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Clinical Psychology
  • Geriatrics and Gerontology
  • Psychiatry and Mental health

Cita questo

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title = "Systemic Immune Responses in Alzheimer’sDisease: In Vitro Mononuclear CellActivation and Cytokine Production",
abstract = "To investigate the systemic signs of immune-inflammatory responses in Alzheimer’s disease (AD), in the present studywe have analyzed blood lymphocyte subsets and the expression of activation markers on peripheral blood mononuclear cells(PBMCs) fromADpatients and age-matched healthy controls (HC) activated in vitro by recombinant amyloid-β peptide (rAβ42).Our study of AD lymphocyte subpopulations confirms the already described decrease of the absolute number and percentage ofB cells when compared to HC lymphocytes, whereas the other subsets are not significantly different in patients and controls.We report the increased expression of the activation marker CD69 and of the chemokine receptors CCR2 and CCR5 on T cellsbut no changes of CD25 after activation. B cells are also activated by rAβ42 as demonstrated by the enhanced expression ofCCR5. Moreover, rAβ42 induces an increased expression of the scavenger receptor CD36 on monocytes. Some activationmarkers and chemokine receptors are overexpressed in unstimulated AD cells when compared to controls. This is evidence ofthe pro-inflammatory status of AD. Stimulation by rAβ42 also induces the production of the pro-inflammatory cytokines IL-1β,IL-6, IFN-γ, and TNF-α, and of the anti-inflammatory cytokines IL-10 and IL-1Ra. The chemokines RANTES, MIP-1β, andeotaxin as well as some growth factors (GM-CSF, G-CSF) are also overproduced by AD-derived PBMC activated by rAβ42.These results support the involvement of systemic immunity in AD patients. However, our study is an observational one so wecannot draw a conclusion about its contribution to the pathophysiology of the disease.",
author = "Domenico Lio and Matteo Bulati and Sonya Vasto and Gabriella Misiano and {Colonna Romano}, Giuseppina and Mario Barbagallo and Calogero Caruso and Giuseppina Candore and {Di Prima}, Anna and Domenico Nuzzo and Pasquale Picone and {Di Carlo}, Marta and Silvio Buffa and Mariavaleria Pellicano'",
year = "2010",
language = "English",
volume = "21",
pages = "181--192",
journal = "Journal of Alzheimer's Disease",
issn = "1387-2877",
publisher = "IOS Press",

}

TY - JOUR

T1 - Systemic Immune Responses in Alzheimer’sDisease: In Vitro Mononuclear CellActivation and Cytokine Production

AU - Lio, Domenico

AU - Bulati, Matteo

AU - Vasto, Sonya

AU - Misiano, Gabriella

AU - Colonna Romano, Giuseppina

AU - Barbagallo, Mario

AU - Caruso, Calogero

AU - Candore, Giuseppina

AU - Di Prima, Anna

AU - Nuzzo, Domenico

AU - Picone, Pasquale

AU - Di Carlo, Marta

AU - Buffa, Silvio

AU - Pellicano', Mariavaleria

PY - 2010

Y1 - 2010

N2 - To investigate the systemic signs of immune-inflammatory responses in Alzheimer’s disease (AD), in the present studywe have analyzed blood lymphocyte subsets and the expression of activation markers on peripheral blood mononuclear cells(PBMCs) fromADpatients and age-matched healthy controls (HC) activated in vitro by recombinant amyloid-β peptide (rAβ42).Our study of AD lymphocyte subpopulations confirms the already described decrease of the absolute number and percentage ofB cells when compared to HC lymphocytes, whereas the other subsets are not significantly different in patients and controls.We report the increased expression of the activation marker CD69 and of the chemokine receptors CCR2 and CCR5 on T cellsbut no changes of CD25 after activation. B cells are also activated by rAβ42 as demonstrated by the enhanced expression ofCCR5. Moreover, rAβ42 induces an increased expression of the scavenger receptor CD36 on monocytes. Some activationmarkers and chemokine receptors are overexpressed in unstimulated AD cells when compared to controls. This is evidence ofthe pro-inflammatory status of AD. Stimulation by rAβ42 also induces the production of the pro-inflammatory cytokines IL-1β,IL-6, IFN-γ, and TNF-α, and of the anti-inflammatory cytokines IL-10 and IL-1Ra. The chemokines RANTES, MIP-1β, andeotaxin as well as some growth factors (GM-CSF, G-CSF) are also overproduced by AD-derived PBMC activated by rAβ42.These results support the involvement of systemic immunity in AD patients. However, our study is an observational one so wecannot draw a conclusion about its contribution to the pathophysiology of the disease.

AB - To investigate the systemic signs of immune-inflammatory responses in Alzheimer’s disease (AD), in the present studywe have analyzed blood lymphocyte subsets and the expression of activation markers on peripheral blood mononuclear cells(PBMCs) fromADpatients and age-matched healthy controls (HC) activated in vitro by recombinant amyloid-β peptide (rAβ42).Our study of AD lymphocyte subpopulations confirms the already described decrease of the absolute number and percentage ofB cells when compared to HC lymphocytes, whereas the other subsets are not significantly different in patients and controls.We report the increased expression of the activation marker CD69 and of the chemokine receptors CCR2 and CCR5 on T cellsbut no changes of CD25 after activation. B cells are also activated by rAβ42 as demonstrated by the enhanced expression ofCCR5. Moreover, rAβ42 induces an increased expression of the scavenger receptor CD36 on monocytes. Some activationmarkers and chemokine receptors are overexpressed in unstimulated AD cells when compared to controls. This is evidence ofthe pro-inflammatory status of AD. Stimulation by rAβ42 also induces the production of the pro-inflammatory cytokines IL-1β,IL-6, IFN-γ, and TNF-α, and of the anti-inflammatory cytokines IL-10 and IL-1Ra. The chemokines RANTES, MIP-1β, andeotaxin as well as some growth factors (GM-CSF, G-CSF) are also overproduced by AD-derived PBMC activated by rAβ42.These results support the involvement of systemic immunity in AD patients. However, our study is an observational one so wecannot draw a conclusion about its contribution to the pathophysiology of the disease.

UR - http://hdl.handle.net/10447/59405

M3 - Article

VL - 21

SP - 181

EP - 192

JO - Journal of Alzheimer's Disease

JF - Journal of Alzheimer's Disease

SN - 1387-2877

ER -