The Th17/Treg imbalance and cytokine environment in peripheral blood of patients with rheumatoid arthritis

Abstract

Broken Th17/Treg balance has been reported contributing to several inflammatory autoimmune diseases. The objective of the study was to investigate whether the Th17/Treg balance was impaired in the peripheral blood of patients with rheumatoid arthritis (RA). The frequencies of Treg cells and Th17 cells and mRNA expression of transcription factor RORγt and FoxP3 in peripheral blood of RA patients (n = 37) and healthy controls (n = 30) were determined by flow cytometry and real-time PCR, respectively. Eleven serum cytokines were analyzed by using cytometeric bead array (CBA). The results demonstrated that active RA patients exhibited increased peripheral Th17 cells, Th1- and Th17-related cytokines and RORγt expression while decreased Treg cells and FoxP3 expression. In addition, Th17/Treg ratios were positively correlated with serum concentrations of Th1- and Th17-related cytokines. In conclusion, our results indicated that Th17/Treg balance was broken in peripheral blood, which may play an important role in the development of RA.

The use of Mycobacterium tuberculosis HspX and GlcB proteins to identify latent tuberculosis in rheumatoid arthritis patients

“…Th17 and Treg cells can be induced by IL-6 and previous studies have reported that this cytokine was significantly elevated in patients with TB and RA ( Okada et al 2011 , Wang et al 2012 , Zhang et al 2012 ). IL-6 is involved in the pathogenesis of RA and contributes to tissue destruction.…”

“…It is believed that the Th1 and Th17 cell subtypes are mainly responsible for the inflammatory responses in this disease ( Chabaud et al 1999 , Cope 2008 ). Recent studies have indicated that imbalances of Th1/Th2 and Th17/Treg cells may be responsible for the development and progression of RA ( Boissier et al 2008 , Wang et al 2012 ).…”

Vogt-Koyanagi-Harada Disease Associated with Rheumatoid Arthritis

“…furthermore, Th1-and T17-related cytokine dominance has also been demonstrated for both diseases. [7,8] ımmunogenetic analysis has indicated a strong association between HlA and VKH, including HlA-DR4, HlA-DRb1, and HlADRw53. ın fact, HlADRb1*0405, one of the subtypes of DR4, is the most frequently found genetic allele in VKH patients.…”

“…[7] Similarly, it has been demonstrated that the frequency of Th1 and T17 cells is significantly higher in the peripheral blood of RA patients than in healthy controls, whereas Th2 and Treg cells showed some degree of decrease. [8] T helper cell subsets secrete different cytokines which regulate leukocyte trafficking under physiological and pathological conditions. furthermore, Th1-and T17-related cytokine dominance has also been demonstrated for both diseases.…”

APL1, an altered peptide ligand derived from human heat-shock protein 60, increases the frequency of Tregs and its suppressive capacity against antigen responding effector CD4 + T cells from rheumatoid arthritis patients

“…A subset of CD4 effector T helper cells that produce IL-17, termed T helper 17 (Th17) cells, has been implicated as the pivotal driving force of autoimmune inflammation in several human autoimmune diseases (Waite and Skokos 2012). A novel hypothesis suggests that a Th17/regulatory T-cell (Treg) imbalance may be responsible for the development and progression of RA (Wang et al 2012;AlFadhli 2013). Expression levels of IL-17 have been found increased in RA synovium (Kotake et al 1999), as well as in peripheral blood mononuclear cells (PBMCs) supernatants from patients compared with healthy controls (Shen et al 2010).…”