The relation between trail (TNF related apoptosis inducing ligand) ligand and receptor profile and rheumatoid arthritis

Rheumatoid Arthritis (RA) is the most common, chronic autoimmune inflammatory disorder. Although the pathogenesis of disease is unclear, it is well known that T cells play a major role in both development and perpetuation of RA through activating macrophages and B cells. Apoptosis or programmed cell death regulates central and peripheral T cells activity during the immune response. Since the lack of TNF-Related Apoptosis Inducing Ligand (TRAIL) expression resulted in defective thymocyte apoptosis leading to an autoimmune disease, we explored evidence for alterations in TRAIL/TRAIL receptors? expression on peripheral T lymphocytes in the molecular mechanism of RA development.Accordingly, we performed a flow cytometric analysis to examine the T cell associated TRAIL and its receptors expression profile in patients with RA. Significant up-regulation of TRAIL and its receptors (both death and decoy) was detected on both CD4+ and CD8+ T cells in RA patients compared to control individuals. The correlation between TRAIL and its? receptor expression profile was compared with clinical RA parameters such as RA activity (DAS28) scoring. Intriguingly, only the CD8+ T cell associated DR4 death receptor and both decoy receptors (DcR1 and DcR2) displayed a positive correlation with patients? DAS scores.In conclusion, differential alteration of TRAIL death and decoy receptor expression profiles on T cells indicates that these profiles might be important in revelation of RA pathogenesis.