scholarly journals Frequency and phenotype of peripheral blood Th17 cells in ankylosing spondylitis and rheumatoid arthritis

2009 ◽  
Vol 60 (6) ◽  
pp. 1647-1656 ◽  
Author(s):  
Hui Shen ◽  
Jane C. Goodall ◽  
J. S. Hill Gaston
Keyword(s):  
Rheumatoid Arthritis ◽  
Ankylosing Spondylitis ◽  
Peripheral Blood ◽  
Th17 Cells

scholarly journals Increased Frequencies of Th22 Cells as well as Th17 Cells in the Peripheral Blood of Patients with Ankylosing Spondylitis and Rheumatoid Arthritis

PLoS ONE ◽  
2012 ◽  
Vol 7 (4) ◽  
pp. e31000 ◽  
Author(s):  
Lei Zhang ◽  
Yong-gang Li ◽  
Yu-hua Li ◽  
Lei Qi ◽  
Xin-guang Liu ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Ankylosing Spondylitis ◽  
Peripheral Blood ◽  
Th17 Cells ◽  
Th22 Cells

THU0129 Selective elimination of pathogenic TH17 cells from peripheral blood of rheumatoid arthritis patients by a purified fungal polysaccharide

2013 ◽  
Vol 71 (Suppl 3) ◽  
pp. 198.3-198
Author(s):  
A. Alunno ◽  
E. Pericolini ◽  
E. Gabrielli ◽  
O. Bistoni ◽  
S. Caterbi ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Peripheral Blood ◽  
Th17 Cells ◽  
Selective Elimination

Cytokine Secretion by Pathogen Recognition Receptor-stimulated Dendritic Cells in Rheumatoid Arthritis and Ankylosing Spondylitis

2012 ◽  
Vol 39 (10) ◽  
pp. 1918-1928 ◽  
Author(s):  
CLAUDIA PREVOSTO ◽  
JANE C. GOODALL ◽  
J.S. HILL GASTON
Keyword(s):  
Rheumatoid Arthritis ◽  
Dendritic Cells ◽  
Ankylosing Spondylitis ◽  
Messenger Rna ◽  
Posttranscriptional Regulation ◽  
Th17 Cells ◽  
Cytokine Secretion ◽  
Pathogen Recognition ◽  
Interleukin 23 ◽  
Factor Α

Objective.Interleukin 23 (IL-23) plays a major role in differentiation and survival of IL-17-secreting CD4+ Th17 cells. Having noted a higher frequency of Th17 cells in ankylosing spondylitis (AS) and rheumatoid arthritis (RA) than in healthy donors (HD), we investigated whether IL-23 secretion is increased in these conditions.Methods.Monocyte-derived dendritic cells (moDC) were obtained from peripheral blood of 17 HD, 16 patients with RA, and 30 patients with AS, and stimulated with ligands for several pathogen recognition receptors. Messenger RNA (mRNA) expression and cytokine secretion were analyzed by real-time polymerase chain reaction and ELISA, respectively.Results.The combination of ligands for Toll-like receptors (TLR) 7/8 and TLR3 led to synergistic secretion of both IL-23 and IL-12p70 from all subjects; similar synergy was seen with TLR2 ligands and curdlan. However, for both combinations, moDC from patients with RA produced significantly lower amounts of IL-23 than moDC from patients with AS; in contrast, IL-12p70 secretion did not differ. Similarly, tumor necrosis factor-α, IL-6, and IL-10 were secreted at comparable levels in all subjects, whereas CXCL8 and CCL3 production was actually enhanced in moDC of patients with RA. Equivalent levels of mRNA for both IL-23p19 and IL-12p35 subunits were found in moDC from all donors, suggesting posttranscriptional regulation of IL-23 production in RA.Conclusion.Our observations show that IL-23 production is decreased in RA and maintained in AS. Because increased numbers of CD4+IL-17+ T cells are seen in both diseases, these observations imply that there are different mechanisms underlying chronic inflammation in these 2 forms of inflammatory arthritis.

scholarly journals Effect of IL-34 on T helper 17 cell proliferation and IL-17 secretion by peripheral blood mononuclear cells from rheumatoid arthritis patients

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Xin Li ◽  
Yimeng Lei ◽  
Ziyu Gao ◽  
Bei Zhang ◽  
Liping Xia ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Transcription Factor ◽  
Peripheral Blood ◽  
Th17 Cells ◽  
Mononuclear Cells ◽  
Treg Cells ◽  
T Helper ◽  
T Helper 17 ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells

AbstractInterleukin (IL)-34 is a new pro-inflammatory cytokine with elevated expression in rheumatoid arthritis (RA) patients. Our previous study showed that the frequency of T helper 17 (Th17) cells was also elevated in RA patients. Our study aimed to determine the effects of IL-34 on the proliferation, transcription factor expression and cytokine secretion of different subgroups of CD4 + T cells [Th1, Th2, Th17 and regulatory T (Treg) cells] in RA patients. Peripheral blood mononuclear cells (PBMCs) were isolated from the peripheral blood of 10 RA patients and stimulated with different concentrations of recombinant human (rh) IL-34 (0, 25, 50 and 100 ng/ml). Flow cytometry was used to determine the frequencies of the 4 subgroups of CD4 + T cells. Reverse transcription-PCR, western blotting and enzyme-linked immunosorbent assays were used to determine the mRNA and protein expression levels of transcription factors and cytokines. As a result, the frequency of Th17 cells was obviously increased under IL-34 stimulation. Moreover, the expression of the transcription factor retinoic acid-related orphan receptor (ROR-γt) and secretion of IL-17 by PBMCs were increased by stimulation with IL-34. However, there were no effects of IL-34 on transcription factors or cytokine secretion in Th1, Th2 and Treg cells. In conclusion, IL-34 can improve the proliferation of Th17 cells and expression of IL-17 in RA patients.

scholarly journals Elevated Ratio of Th17 Cell-Derived Th1 Cells (CD161+Th1 Cells) to CD161+Th17 Cells in Peripheral Blood of Early-Onset Rheumatoid Arthritis Patients

2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Shigeru Kotake ◽  
Yuki Nanke ◽  
Toru Yago ◽  
Manabu Kawamoto ◽  
Tsuyoshi Kobashigawa ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Articular Cartilage ◽  
Peripheral Blood ◽  
Early Onset ◽  
Early Phase ◽  
Th17 Cell ◽  
Th17 Cells ◽  
Chronic Inflammatory Disease ◽  
Helper T Cells ◽  
Th1 Cells

Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by the destruction of articular cartilage and bone with elevated levels of proinflammatory cytokines. It has been reported that IL-17 and Th17 cells play important roles in the pathogenesis of RA. Recently, plasticity in helper T cells has been demonstrated; Th17 cells can convert to Th1 cells. It remains to be elucidated whether this conversion occurs in the early phase of RA. Here, we tried to identify Th17 cells, Th1 cells, and Th17 cell-derived Th1 cells (CD161+Th1 cells) in the peripheral blood of early-onset RA patients. We also evaluated the effect of methotrexate on the ratio of Th17 cells in early-onset RA patients. The ratio of Th17 cell-derived Th1 cells to CD161+Th17 cells was elevated in the peripheral blood of early-onset RA patients. In addition, MTX reduced the ratio of Th17 cells but not Th1 cells. These findings suggest that IL-17 and Th17 play important roles in the early phase of RA; thus, anti-IL-17 antibodies should be administered to patients with RA in the early phase.

scholarly journals TNF-α Inhibitors Decrease Classical CD14hiCD16− Monocyte Subsets in Highly Active, Conventional Treatment Refractory Rheumatoid Arthritis and Ankylosing Spondylitis

2019 ◽  
Vol 20 (2) ◽  
pp. 291 ◽  
Author(s):  
Bogdan Batko ◽  
Agata Schramm-Luc ◽  
Dominik Skiba ◽  
Tomasz Mikolajczyk ◽  
Mateusz Siedlinski
Keyword(s):  
Rheumatoid Arthritis ◽  
Ankylosing Spondylitis ◽  
Disease Activity ◽  
Peripheral Blood ◽  
Peripheral Blood Monocyte ◽  
Placebo Treatment ◽  
Prior History ◽  
Monocyte Subset ◽  
Highly Active ◽  
Tnf Α

Monocytes are pivotal cells in inflammatory joint diseases. We aimed to determine the effect of TNF-α inhibitors (TNFi) on peripheral blood monocyte subpopulations and their activation in ankylosing spondylitis (AS) and rheumatoid arthritis (RA) patients with high disease activity. To address this, we studied 50 (32 AS, 18 RA) patients with highly active disease with no prior history of TNFi use who were recruited and assigned to TNFi or placebo treatment for 12 weeks. Cytometric and clinical assessment was determined at baseline, four, and 12 weeks after initiation of TNFi treatment. We observed that treatment with TNFi led to a significant decrease in CD14hiCD16− monocytes in comparison to placebo, while circulating CD14dimCD16+ monocytes significantly increased. The TNFi-induced monocyte subset shifts were similar in RA and AS patients. While the percentage of CD14dimCD16+ monocytes increased, expression of CD11b and CD11c integrins on their surface was significantly reduced by TNFi. Additionally, CD45RA+ cells were more frequent. The shift towards nonclassical CD14dimCD16+ monocytes in peripheral blood due to TNFi treatment was seen in both AS and RA. This may reflect reduced recruitment of these cells to sites of inflammation due to lower inflammatory burden, which is associated with decreased disease activity.

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