Analysis of Programmed Death-1 in Patients with Psoriatic Arthritis

• Published in: Inflammation Vol. 38; no. 4; pp. 1573 - 1579
• Main Authors: Peled, Michael, Strazza, Marianne, Azoulay-Alfaguter, Inbar, Mor, Adam
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.08.2015; Springer Nature B.V
• Subjects: Adult; Aged; Arthritis, Psoriatic - diagnosis; Arthritis, Psoriatic - metabolism; Biomarkers - metabolism; Biomedical and Life Sciences; Biomedicine; Case-Control Studies; Cells, Cultured; Female; Humans; Immunology; Internal Medicine; Male; Middle Aged; Pathology; Pharmacology/Toxicology; Programmed Cell Death 1 Receptor - biosynthesis; Rheumatology; Young Adult; PD-1; signaling; psoriatic arthritis
• ISSN: 0360-3997; 1573-2576; 1573-2576
• DOI: 10.1007/s10753-015-0132-2

Programmed death-1 (PD-1) is an inhibitory co-receptor that is highly expressed in T lymphocytes that has been shown to downregulate inflammatory responses in several inflammatory diseases including systemic lupus erythematosus and rheumatoid arthritis. Yet, the role of PD-1 in psoriatic arthritis (PsA) has not been studied. In order to fill this gap, we measured the expression levels of PD-1 in peripheral T cells from patients with active disease. Twenty patients and fifteen age-matched healthy control subjects were recruited. The percentage of CD3 + PD-1 + T cells was measured by flow cytometry. Despite normal concentration of peripheral T cells, the expression levels of PD-1 were significantly higher in patients compared to healthy controls. Interestingly, among the patients, the expression levels inversely correlated with disease activity measured by disease activity scores (DAS28). PD-1 expression levels strongly correlated with the number of tender and swollen joints, but not with C-reactive protein (CRP) levels or psoriasis area and severity index (PASI). Functionally, in vitro ligation of PD-1 receptor in PsA T cells inhibited interleukin-2 (IL-2) secretion, Akt phosphorylation, and Rap1 activation. These findings suggest that PD-1 might serve as a biomarker for disease activity in PsA and highlight the need for additional studies in order to establish the role of PD-1 in PsA pathogenesis.