Table of Contents Author Guidelines Submit a Manuscript
Journal of Biomedicine and Biotechnology
Volume 2009, Article ID 406136, 6 pages
http://dx.doi.org/10.1155/2009/406136
Research Article

Variable Increased Expression of Program Death-1 and Program Death-1 Ligands on Peripheral Mononuclear Cells Is Not Impaired in Patients with Systemic Lupus Erythematosus

Section of Rheumatology and Immunology, Department of Internal Medicine, Medical College, National Cheng Kung University, Tainan 704, Taiwan

Received 9 February 2009; Revised 16 June 2009; Accepted 27 June 2009

Academic Editor: Robert E. Cone

Copyright © 2009 Ming-Fei Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Programmed death-1 (PD-1) was shown to deliver an inhibitory signal after binding to its ligands, PD-L1 (B7-H1) or PD-L2 (B7-DC). Recently, up-regulated expression of PD-1 molecule and/or its ligands was demonstrated in human diseases including rheumatoid arthritis and inflammatory colitis. The study aimed to investigate the expression and function of PD-1 and PD-1 ligands on circulating T cells, B cells and monocytes from patient with systemic lupus erythematosus (SLE). The results showed that patients with SLE had significantly increased percentages of PD-1-expressing CD T cells and CD B cells, PD-L1-expressing CD B cells and PD-L2-expressing CD B monocytes. In selected SLE patients and normal subjects, functional study of PD-1/ PD-1 ligands pathway on the production of cytokines by stimulated PBMC was examined. Blockages of PD-1 or PD-1 ligands substantially increased the production of IL-2, IFN- and IL-10, the amplitude of increase roughly ranged from one to three times. There were no significant differences of the enhancing effects on cytokine production by blockage of PD-1/PDL pathway between SLE patients and normal subjects. The study indicates that there are no intrinsically defective expression and function of PD-1 and PD-1 ligands on PBMC in patients with SLE.