Streptococcal-related antigens stimulate production of IL6 and interferon-γ by T cells from patients with Behcet's disease

1992 ◽  
Vol 140 (2) ◽  
pp. 410-419 ◽  
Author(s):  
Shunsei Hirohata ◽  
Hiroshi Oka ◽  
Yutaka Mizushima
2012 ◽  
Vol 168 (1) ◽  
pp. 68-74 ◽  
Author(s):  
J. Shimizu ◽  
K. Takai ◽  
N. Fujiwara ◽  
N. Arimitsu ◽  
Y. Ueda ◽  
...  

The Lancet ◽  
1996 ◽  
Vol 347 (9015) ◽  
pp. 1631-1632 ◽  
Author(s):  
J.S.H. Gaston ◽  
Adam Hasan ◽  
Farida Fortune ◽  
Amanda Wilson ◽  
Thomas Lehner

2021 ◽  
Vol 101 ◽  
pp. 108237
Author(s):  
Samaneh Abbasian ◽  
Mohammad Sadegh Soltani-Zangbar ◽  
Alireza Khabbazi ◽  
Rojin Farzaneh ◽  
Aida Malek Mahdavi ◽  
...  

1986 ◽  
Vol 29 (3) ◽  
pp. 371-378 ◽  
Author(s):  
Tsuyoshi Sakane ◽  
Noboru Suzuki ◽  
Yuji Ueda ◽  
Shinsuke Takada ◽  
Yohko Murakawa ◽  
...  

2020 ◽  
Author(s):  
Manyun Xie ◽  
Yan Yang

Background: Previous studies have indicated that Sirtuin 1 (Sirt1) plays an important role in suppressing inflammatory responses in many diseases. However, the Sirt1 levels and role of Sirt1 in ocular Behcet’s disease (OBD) have not been fully elucidated. Objective: To investigate the role of Sirt1 in the pathogenesis of OBD. Methods: Sirt1 and cytokine levels were measured using enzyme-linked immunosorbent assay (ELISA). Cell viability was determined using the Cell Counting Kit-8. The frequencies of Th17 and Th22 cells were detected using flow cytometry. Results: We found decreased expression of Sirt1 in CD4+ T cells obtained from patients with active OBD. SRT1720, an agonist of Sirt1, significantly upregulated Sirt1 expression in CD4+ T cells from patients with active OBD. Sirt1 activation by SRT1720 significantly suppressed the production of interleukin (IL)-17 and IL-22 by CD4+ T cells and inhibited the expansion of Th17 and Th22 cells. Conclusion: Our results suggest that decreased Sirt1 expression might be involved in the pathogenesis of OBD and that activation of Sirt1 might be considered a potential target for OBD.


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