Affiliations: [a] Gruppo di Studio sull'Immunosenescenza, Dipartimento di Biopatologia e Biotecnologie Mediche e Forensi, Università di Palermo, Italy | [b] Dipartimento di Medicina Clinica e delle Patologie Emergenti, Università di Palermo, Italy | [c] Istituto di Biomedicina e Immunologia Molecolare, CNR, Palermo, Italy
Correspondence:
[*]
Correspondence to: Calogero Caruso, MD, Gruppo di Studio sull'Immunosenescenza, Dipartimento di Biopatologia e Biotecnologie Mediche e Forensi, Università di Palermo, Corso Tukory 211, 90134 Palermo, Italy. Tel.: +39 0916555911; Fax: +39 0916555933; E-mail: marcoc@unipa.it.
Abstract: 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-β peptide (rAβ42). 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 rAβ42 as demonstrated by the enhanced expression of CCR5. Moreover, rAβ42 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 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, and eotaxin 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 we cannot draw a conclusion about its contribution to the pathophysiology of the disease.
