Systemic Immune Responses in Alzheimer's Disease: In Vitro Mononuclear Cell Activation and Cytokine Production
Autor: | Matteo Bulati, Anna Di Prima, Sonya Vasto, Mario Barbagallo, Mariavaleria Pellicanò, Silvio Buffa, Marta Di Carlo, Calogero Caruso, Gabriella Misiano, Domenico Lio, Pasquale Picone, Domenico Nuzzo, Giuseppina Colonna-Romano, Giuseppina Candore |
---|---|
Přispěvatelé: | Pellicanò, M, Bulati, M, Buffa, S, Barbagallo, M, Di Prima, A, Misiano, G, Pasquale Picone, P, Di Carlo, M, Nuzzo, D, Candore, G, Vasto, S, Lio, D, Caruso, C, Colonna Romano, G |
Rok vydání: | 2010 |
Předmět: |
Male
Eotaxin CCR2 Chemokine Time Factors medicine.medical_treatment Peripheral blood mononuclear cell Chemokine receptor Immune system Alzheimer’s disease chemokine cytokine PBMC rAβ42 Alzheimer Disease medicine Humans Lymphocytes IL-2 receptor Cells Cultured Aged Settore MED/04 - Patologia Generale Aged 80 and over Analysis of Variance Amyloid beta-Peptides biology business.industry General Neuroscience General Medicine Middle Aged Flow Cytometry Peptide Fragments Psychiatry and Mental health Clinical Psychology Cytokine Gene Expression Regulation Case-Control Studies Immunology Leukocytes Mononuclear biology.protein Cytokines Female Geriatrics and Gerontology business |
Zdroj: | Journal of Alzheimer's Disease. 21:181-192 |
ISSN: | 1875-8908 1387-2877 |
DOI: | 10.3233/jad-2010-091714 |
Popis: | To investigate the systemic signs of immune-inflammatory responses in Alzheimer's disease (AD), in the present study we have analyzed blood lymphocyte subsets and the expression of activation markers on peripheral blood mononuclear cells (PBMCs) from AD patients and age-matched healthy controls (HC) activated in vitro by recombinant amyloid-beta peptide (rAbeta42). Our study of AD lymphocyte subpopulations confirms the already described decrease of the absolute number and percentage of B 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 cells but no changes of CD25 after activation. B cells are also activated by rAbeta42 as demonstrated by the enhanced expression of CCR5. Moreover, rAbeta42 induces an increased expression of the scavenger receptor CD36 on monocytes. Some activation markers and chemokine receptors are overexpressed in unstimulated AD cells when compared to controls. This is evidence of the pro-inflammatory status of AD. Stimulation by rAbeta42 also induces the production of the pro-inflammatory cytokines IL-1beta, IL-6, IFN-gamma, and TNF-alpha, and of the anti-inflammatory cytokines IL-10 and IL-1Ra. The chemokines RANTES, MIP-1beta, and eotaxin as well as some growth factors (GM-CSF, G-CSF) are also overproduced by AD-derived PBMC activated by rAbeta42. These results support the involvement of systemic immunity in AD patients. However, our study is an observational one so we cannot draw a conclusion about its contribution to the pathophysiology of the disease. |
Databáze: | OpenAIRE |
Externí odkaz: |