TIPE2 expression is increased in peripheral blood mononuclear cells from patients with rheumatoid arthritis.

Zhu Shi-Bai,Jiang Chao,Ye Can-Hua,Zhai Jie,Sun Ying-Chuan,Liu Rui-Min,Chen Xi,Qian Wen-Wei

doi:10.18632/oncotarget.21267

Abstract

We investigated the changes in mRNA and protein expression of tumor necrosis factor-α–induced protein 8-like 2 (TIPE2) and PEST-containing nuclear protein (PCNP) in peripheral blood lymphocytes from 54 patients with rheumatoid arthritis (RA) and the spleens of model mice with collagen-induced arthritis (CIA) to generate new ideas for clinical diagnosis and treatment. Expression levels of both TIPE2 and PCNP were higher in RA patients and CIA mice than in their respective controls. They were also higher in the 32 patients with active RA than in the 22 with inactive RA (P < 0.001 for both). After comprehensively treating patients with active RA with anti-inflammatory and antirheumatic drugs for 6 months, they were stable, and there was no difference in TIPE2 levels between the treated patients and those with inactive RA (P = 0.85). In addition, TIPE2 mRNA levels in peripheral blood correlated positively with PCNP (R2 = 0.744, P = 0.001). The DAS28 score correlated positively with peripheral blood TIPE2 levels in the RA patients (R2 = 0.945, P = 0.001). These findings suggest TIPE2 expression increases with the severity of RA.

Highlights

Rheumatoid arthritis (RA) is a multisystem inflammatory autoimmune disease that mainly damages peripheral joints, characterized by synovial tissue inflammatory hyperplasia and progressive destruction of articular cartilage [1]
We investigated the changes in mRNA and protein expression of tumor necrosis factor-α–induced protein 8-like 2 (TIPE2) and PEST-containing nuclear protein (PCNP) in peripheral blood lymphocytes from 54 patients with rheumatoid arthritis (RA) and the spleens of model mice with collagen-induced arthritis (CIA) to generate new ideas for clinical diagnosis and treatment
Recent studies have shown that abnormal expression of TIPE2 is associated with inflammatory diseases, autoimmune diseases such as systemic lupus erythematosus (SLE), asthma, and myasthenia gravis [2,3,4,5], which suggests TIPE2 may play an important role in the pathogenesis of autoimmune disease by maintaining immune homeostasis

Summary

Introduction

Rheumatoid arthritis (RA) is a multisystem inflammatory autoimmune disease that mainly damages peripheral joints, characterized by synovial tissue inflammatory hyperplasia and progressive destruction of articular cartilage [1]. The inflammatory process is complex immune and involves a variety of cytokines, adhesion molecules, and chemokines and multigene synergies. The exact molecular mechanism of RA remains to be confirmed. The identification of new molecules involved in the pathogenesis of RA is essential for development of new treatments. The tumor necrosis factor-α–induced protein 8-like 2 (TIPE2) gene was discovered in 2002; it helps maintain the self-stabilization of the immune system and is a member of the TIPE family. Recent studies have shown that abnormal expression of TIPE2 is associated with inflammatory diseases, autoimmune diseases such as systemic lupus erythematosus (SLE), asthma, and myasthenia gravis [2,3,4,5], which suggests TIPE2 may play an important role in the pathogenesis of autoimmune disease by maintaining immune homeostasis

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Conclusion