C 02 Phenotype and functional profile of T cells expressing TCRγδ receptor from patients with active Behçet's disease (BD)

1993 ◽  
Vol 14 ◽  
pp. 23s
Author(s):  
K. Hamzaoui ◽  
F. Hentati ◽  
A. Hamzaoui ◽  
A. Chabbou ◽  
M. Ben Hamida ◽  
...  
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.


1999 ◽  
Vol 8 (2) ◽  
pp. 101-106 ◽  
Author(s):  
K. Hamzaoui ◽  
A. Hamzaoui ◽  
L. Zakraoui ◽  
A. Chabbou

Behçet's disease (BD) is a current systemic vasculitis of unknown aetiology. Eyes, skin, joints, the oral cavity, genital system, blood vessels, central nervous system and lung are usually involved. Defective regulation of programmed cell death (apoptosis) may play a role in the development of (BD), and the protooncogene Bcl-2 is involved in the control of apoptosis in immunocompetent cells. We therefore wished to investigate the expression of Bcl-2 in the peripheral lymphocytes and in two inflammatory sites of patients with active BD: bronchoalveolar lavage (BAL) and cerebrospinal fluid (CSF) lymphocytes. Levels of Bcl-2 expression in the lymphocytes of patients with BD and, for comparison, in the lymphocytes of healthy controls and non-inflammatory neurological diseases (NIND), were studied by two-colour cytofluorography and RNA analysis. In BD patients, a significant proportion of T cells expressed increased amounts of Bcl-2 protein, both in peripheral blood and in inflammatory sites. Mononuclear cells of patients with BD showed increased amount of Bcl-2 messenger RNA. The in vitro incubation of T lymphocytes with IL-10, significantly increased the Bcl-2 expression, specifically in T lymphocytes from inflammatory sites. In active BD, stimulation of HSV-1 T lymphocytes slightly increased Bcl-2 expression, not significantly different from unstimulated HSV-1 T cells. The occurrence of circulating T lymphocytes with abnormally high Bcl-2 expression in peripheral circulation and in inflammatory sites may be explained in part by the increasedin vivoactivation levels, and by aetiopathological agent(s): our findings seem to indicate an important role in the chronic inflammation in BD.


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