Enhanced HMGB1 Expression May Contribute to Th17 Cells Activation in Rheumatoid Arthritis

نویسندگان

  • Yan Shi
  • Siamak Sandoghchian Shotorbani
  • Zhaoliang Su
  • Yanfang Liu
  • Jia Tong
  • Dong Zheng
  • Jianguo Chen
  • Yingzhao Liu
  • Yan Xu
  • Zhijun Jiao
  • Shengjun Wang
  • Liwei Lu
  • Xinxiang Huang
  • Huaxi Xu
چکیده

Rheumatoid arthritis(RA) is a common autoimmune disease associated with Th17 cells, but what about the effect of high-mobility group box chromosomal protein 1 (HMGB1) and the relationship between Th17-associated factors and HMGB1 in RA remains unknown. In the present study, we investigated the mRNA levels of HMGB1, RORγt, and IL-17 in peripheral blood mononuclear cells (PBMCs) from patients with rheumatoid arthritis by quantitative real-time PCR (RT-qPCR), and the concentrations of HMGB1, IL-17, and IL-23 in plasma were detected by ELISA. And then, the effect of HMGB1 on Th17 cells differentiation was analyzed in vitro. Our clinical studies showed that the mRNAs of HMGB1, RORγt, and IL-17 in patients were higher than that in health control (P < 0.05), especially in active RA patients (P < 0.05). The plasma HMGB1, IL-17, and IL-23 in RA patients were also higher than that in health control (P < 0.05); there was a positive correlation between the expression levels of HMGB1 and the amount of CRP, ERS, and RF in plasma. In vitro, the IL-17-produced CD4(+)T cells were increased with 100 ng/mL rHMGB1 for 12h, which indicated that the increased HMGB1 might contribute to Th17 cells activation in RA patients.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Activation of Toll-Like Receptors 2 by High-Mobility Group Box 1 in Monocytes from Patients with Ischemic Stroke

Background: Stroke is a leading cause of death all around the world, and ischemic stroke is considered to be the most common stroke type. Toll-like receptors (TLRs) are important molecules for detection of both pathogen invasion and tissue damage. In this regard, the purpose of this study was to assess the expression level of TLR2 on monocytes in patients with ischemic stroke and to evaluate th...

متن کامل

Evaluation of Beclin-1 and Atg5 genes expression levels in peripheral blood cells of patients with rheumatoid arthritis

Background: Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease, which primarily affects the joints. During RA development, T cells and other immune cells are recruited to the synovial tissue and promote RA. Autophagy is a process in which intracellular organelles and compounds are degraded. Autophagy as a regulator of cell homeostasis can affect immune cells activation and c...

متن کامل

High mobility group box 1 potentiates the pro-inflammatory effects of interleukin-1β in osteoarthritic synoviocytes

INTRODUCTION High mobility group box 1 (HMGB1) is released by necrotic cells or secreted in response to inflammatory stimuli. Extracellular HMGB1 may act as a pro-inflammatory cytokine in rheumatoid arthritis. We have recently reported that HMGB1 is released by osteoarthritic synoviocytes after activation with interleukin-1beta (IL-1β) The present study investigated the role of HMGB1 in synovia...

متن کامل

A Flowcytometry Study of CD55 and CD59 Expression on Erythrocytes in Rheumatoid Arthritis Patients

Background: Inappropriate activation or blockage of the inhibition of complement system could cause tissue damages in autoimmune diseases particularly rheumatoid arthritis (RA). Defect in complement component regulation may cause damages to tissues, on the other hand, or the damaged tissue might affect the unnecessary activation of complement components.   Objective: To investigate the expressi...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 2012  شماره 

صفحات  -

تاریخ انتشار 2012