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Journal of Biomedicine and Biotechnology
Volume 2012, Article ID 535361, 6 pages
http://dx.doi.org/10.1155/2012/535361
Research Article

Comprehensive Evaluation of Different T-Helper Cell Subsets Differentiation and Function in Rheumatoid Arthritis

Department of Rheumatology, The Second Hospital of Shanxi Medical University, Shanxi, Taiyuan 030001, China

Received 14 March 2012; Revised 21 May 2012; Accepted 5 June 2012

Academic Editor: Soldano Ferrone

Copyright © 2012 Junwei Chen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Rheumatoid arthritis (RA) is the most common autoimmune disorder. Loss of Th1/Th2 and Th17/Treg balance has been reported in several inflammatory autoimmune diseases. This study was to investigate Th1, Th2, Th17, and Treg differentiation and related cytokines in RA patients. The frequencies of Th1, Th2, Th17, and Treg cells in peripheral blood of RA patients ( 𝑛 = 7 6 ) and healthy controls ( 𝑛 = 1 8 ) were determined by flow cytometry. Eight serum cytokines were analyzed using cytometric bead array. The results demonstrated that RA patients exhibited increased peripheral Th1/Th17 cells and Th1/Th17-related cytokines. However, Th1 cells only reached significant difference at advanced stage, but Th17 at all stages, suggesting more important roles in Th17 cells. For Th2 and Treg cells, there was a different function pattern in RA progression. Although with the increase of DAS28 score, Th2 cell experienced some degree of decrease in RA patients, no significant difference was observed. IL-4 and IL-10 showed a significant increase in RA patients. These indicated that Th2 cells might exert immunosuppression effects mainly by secreting cytokines. Treg cells were found significantly decreased in RA patients, but no difference was observed in TGF-β expression, indicating a cell-cell interaction pattern in Treg cell.