Elevated Serum Levels of Soluble CD30 in Ankylosing Spondylitis Patients and Its Association with Disease Severity-Related Parameters.

Rongfen Gao,Lingli Dong,Yu Chen,Wei Sun,Yuying Su,Chenqiong Wang

doi:10.1155/2015/617282

Abstract

Soluble CD30 (sCD30), a transmembrane glycoprotein that belongs to the tumor necrosis factor receptor (TNFR) superfamily, has been shown to be associated with various pathological conditions. This study was designed to measure the levels of serum sCD30 in patients with ankylosing spondylitis (AS) and to evaluate the relationships between serum sCD30 levels and other disease severity-related indexes, including bath ankylosing spondylitis disease activity index (BASDAI), ankylosing spondylitis disease activity score (ASDAS), and bath ankylosing spondylitis functional index (BASFI). Our results demonstrated significantly elevated sCD30 levels in AS patients compared to healthy controls (HCs) with mean values of 32.0 ± 12.2 and 24.9 ± 8.0 ng/mL, respectively (P ** = 0.007), suggesting a potential role of sCD30 in the pathogenesis of AS. However, no significant correlations of sCD30 with BASDAI, ASDAS, or BASFI were detected in our study (P > 0.05). Therefore, sCD30 cannot be used as a reliable marker for reflecting disease activity and functional ability of AS patients.

Highlights

Ankylosing spondylitis (AS) is a chronic inflammatory disorder that mainly affects the sacroiliac joints and axial skeleton of young males
Our results revealed a statistically significant increase of serum Soluble CD30 (sCD30) levels in AS patients compared to healthy controls (HCs) (32.0 ± 12.2 and 24.9 ± 8.0 ng/mL, resp.; Figure 1(a))
The small number of patients treated with disease modifying antirheumatic drugs (DMARDs) or glucocorticoids made it impossible to assess the effects of the drugs on serum sCD30 levels, and, a future prospective study is needed

Summary

Introduction

Ankylosing spondylitis (AS) is a chronic inflammatory disorder that mainly affects the sacroiliac joints and axial skeleton of young males. It is known to be a highly genetic disease and there is a strong genetic association of MHC molecules with AS, especially human leukocyte antigen-B27 (HLA-B27) [1]. HLA-B27 is an MHC class I molecule that is highly expressed on antigen presenting cells. Self or bacterial antigen peptides might be presented by HLA-B27 to CD8+ T cells, which would lead to an aberrant immunological response. A recent study found that imbalances in subsets of T cell populations might be responsible for the pathogenesis of AS, including increased ratios of Th1/Th2 and Th17/Treg cells [2]. Abnormal functions of immune cells in patients with AS can lead to the upregulation of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), IL-6, soluble IL-2 receptor, IL-17, and IL-23 [1,2,3]

Methods

Results

Conclusion