Abstract
Rheumatoid arthritis (RA) is a chronic, systematic autoimmune disease that mainly affects joints and bones. Although the precise etiology is still unknown, Th17 cell is being recognized as an important mediator in pathogenesis of RA. VSTM1-v2 is a novel cytokine which has recently been reported to promote the differentiation of Th17 cells. This study is performed to study whether VSTM1-v2 can be recognized as a biomarker of RA, and is correlated to IL-17 expression. We obtained peripheral blood mononuclear cells (PBMCs) from 40 patients with RA and 40 age- and sex- matched healthy controls by standard Ficoll-Paque Plus density centrifugation. The mRNA expression levels of VSTM1-v2 and IL-17A in PBMCs were detected by real time-PCR. Disease activity parameters of RA were measured by routine methods. Our results showed that VSTM1-v2 mRNA expression in PBMCs from RA patients was significantly increased in comparison of that in healthy individuals. The VSTM1-v2 mRNA expression level was positively correlated with IL-17A mRNA expression level, DAS28, CRP and ESR, but was not correlated to RF, Anti-CCP or ANA. VSTM1-v2 might be a biomarker of RA and a novel factor in the pathogenesis of RA.
Highlights
Rheumatoid arthritis (RA), a systematic autoimmune disease, is characterized by infiltration of synovium with immune cells leading to joint destruction [1]
We studied the expression of V-set and transmembrane domain containing 1 (VSTM1)-v2 mRNA in peripheral blood mononuclear cells (PBMCs) from patients with RA, and analyzed the relationship between VSTM1-v2 and IL-17A
As T helper 17 cells (Th17) cells play a central role in pathogenesis of RA and VSTM1-v2 is involved in Th17 cell differentiation, we further detected RNA expression of IL-17A, and analyzed the relationship between expression of VSTM1-v2 and IL-17A in patients with RA
Summary
Rheumatoid arthritis (RA), a systematic autoimmune disease, is characterized by infiltration of synovium with immune cells leading to joint destruction [1]. The pathogenesis of RA is still unclear, many factors such as pro-inflammatory cytokines, immune cells, and genetic factors were considered to be implicated in pathogenesis RA [2]. The discovery of T helper 17 cells (Th17), which are characterized by secreting their signature cytokine IL-17A [3, 4], increased our understanding of the pathogenesis of RA. IL-17A can induce secretion of many pro-inflammatory cytokines from macrophage, and production of autoantibody from B cell[5, 6]. PLOS ONE | DOI:10.1371/journal.pone.0146805 January 13, 2016
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