scholarly journals Pharmacological Inactivation of Src Family Kinases Inhibits LPS-Induced TNF-αProduction in PBMC of Patients with Behçet’s Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Sevgi Irtegun ◽  
Gulsum Pektanc ◽  
Zeynep M. Akkurt ◽  
Mehtap Bozkurt ◽  
Fatih M. Turkcu ◽  
...  
Keyword(s):  
Behçet’S Disease ◽  
Proinflammatory Cytokines ◽  
Behcet’S Disease ◽  
Mononuclear Cells ◽  
Behçet's Disease ◽  
Skin Lesions ◽  
Chronic Inflammatory Disease ◽  
Src Family Kinases ◽  
Peripheral Blood Mononuclear ◽  
Behcet's Disease

Behçet’s disease (BD) is a multisystemic chronic inflammatory disease characterized by relapsing oral and genital ulcers, uveitis, and skin lesions. The pathogenesis of BD is still unknown. Aberrant production of some cytokines/chemokines plays an important role in the pathogenesis of various inflammatory diseases. Revealing a key signaling regulatory mechanism involved in proinflammatory cytokines/chemokines production is critical for understanding of the pathogenesis of BD. The aim of this study was to determine the role of Src family kinases (SFKs) in production of some LPS-induced proinflammatory cytokines/chemokines in peripheral blood mononuclear cells (PBMC) of active BD patients. Chemical inhibition of SFKs activity impaired LPS-induced TNF-αproduction in PBMC of active BD patients, suggesting that modulating SFKs activity may be a potential target for BD treatment.

scholarly journals Behçet's Disease (Adamantiades-Behçet's Disease)

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Fumio Kaneko ◽  
Ari Togashi ◽  
Sanae Saito ◽  
Hideo Sakuma ◽  
Noritaka Oyama ◽  
...  
Keyword(s):  
T Cell ◽  
Behçet’S Disease ◽  
Behcet’S Disease ◽  
Mononuclear Cells ◽  
Behçet's Disease ◽  
Cell Epitope ◽  
T Cell Response ◽  
Delayed Type Hypersensitivity ◽  
Peripheral Blood Mononuclear ◽  
Behcet's Disease

Adamantiades-Behçet's disease (ABD) is characterized by starting with oral aphthous ulceration and developing of the systemic involvements. The pathogenesis of ABD is closely correlated with the genetic factors and the triggering factors which acquire delayed-type hypersensitivity reaction against oralstreptococcimediated by IL-12 cytokine family. HLA-B51 is associated in more than 60% of the patients and its restricted CD8+ T cell response is clearly correlated with the target tissues.Bes-1gene encoded partialS. sanguinisgenome which is highly homologous with retinal protein, and 65 kD heat shock protein (Hsp-65) released from streptococci is playing an important role with human Hsp-60 in the pathogenesis of ABD. Although Hsp-65/60 has homologies with the respective T cell epitope, it stimulates peripheral blood mononuclear cells (PBMCs) from ABD patients. On the other hand, some peptides of Hsp-65 were found to reduce IL-8 and IL-12 production from PBMCs of ABD patients in active stage.

scholarly journals Behçet’s Disease as a Model of Venous Thrombosis

2010 ◽  
Vol 4 (1) ◽  
pp. 71-77 ◽  
Author(s):  
Micaela La Regina ◽  
Armen Yuri Gasparyan ◽  
Francesco Orlandini ◽  
Domenico Prisco
Keyword(s):  
Venous Thrombosis ◽  
Behçet’S Disease ◽  
Behcet’S Disease ◽  
Behçet's Disease ◽  
Skin Lesions ◽  
Chronic Inflammatory Disease ◽  
Vascular Lesions ◽  
Behcet's Disease ◽  
Therapeutic Measures ◽  
Arterial Aneurysms

Behçet’s disease (BD) is a chronic inflammatory disease of unknown aetiology characterized by recurrent oral, genital aphthous ulcerations, uveitis, skin lesions and other multisystem affections associated with vasculitis. Different types of vessels, predominantly veins, can be affected in BD. The frequency of vascular lesions in BD, such as superficial and deep venous thromboses, arterial aneurysms and occlusions, ranges between 7-29%. In this review, various factors of thrombogenesis in BD, particularly pro- and antithrombotic endothelial and non-endothelial factors, factors of coagulation, platelet activation and rheological changes are presented and discussed from positions of Virchow’s triad of venous thrombosis. Despite advances in understanding of thrombogenesis in BD, still many issues of diagnosis and targeted preventive and therapeutic measures remain unresolved. Further studies are needed to clarify the pathobiology of BD-related thrombosis and to provide the clinicians with recommendations over the utility, safety and effectiveness of the antithrombotic therapy in BD.

Decreased expression of A20 is associated with ocular Behcet’s disease (BD) but not with Vogt-Koyanagi-Harada (VKH) disease

2018 ◽  
Vol 102 (8) ◽  
pp. 1167-1172 ◽  
Author(s):  
Yue He ◽  
Chaokui Wang ◽  
Guannan Su ◽  
Bolin Deng ◽  
Zi Ye ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
T Cells ◽  
Behçet’S Disease ◽  
Behcet’S Disease ◽  
Mononuclear Cells ◽  
Behçet's Disease ◽  
Normal Subjects ◽  
Peripheral Blood Mononuclear ◽  
Behcet's Disease ◽  
Vkh Disease

PurposeA20 is a ubiquitously expressed and inducible cytosolic protein, which plays an important role in the negative regulation of inflammation and immunity. In this study, we investigated the role of A20 in Behcet’s disease (BD) and Vogt-Koyanagi-Harada (VKH) disease.MethodsThe levels of A20 in peripheral blood mononuclear cells (PBMCs) and dendritic cells (DCs) were detected in BD patients with active and inactive uveitis, VKH patients with active and inactive uveitis, and normal subjects, respectively, by real-time PCR. The effect of A20 silencing was performed by transduction of DCs with adenovirus containing an A20 shRNA vector. The effect of A20 silencing on the maturation of DCs was measured by flow cytometry. The effect of A20 silencing of DCs on cytokine production by DCs and CD4+ T cells was analysed by ELISA. The phosphorylation levels of JNK, p38 and ERK1/2 were detected by flow cytometry.ResultsThe expression of A20 was markedly decreased in PBMCs and DCs obtained from BD patients with active uveitis, but not in patients with VKH disease as compared with normal controls. Silencing of A20 significantly increased the levels of interleukin (IL)-1β and IL-6 and suppressed the expression of the anti-inflammatory cytokines IL-10 and IL-27. Downregulation of A20 also led to an increase in IL-17 production by CD4+ T cells. However, downregulation of A20 in DCs did not have an effect on cell surface markers such as CD40, CD80, CD83, CD86 and HLA-DR. Silencing of A20 caused an increased expression of phospho-JNK and phospho-MAPK p38 but not phospho-ERK1/2.ConclusionsThis study showed that the expression of A20 was decreased in BD patients with active uveitis but not in VKH disease. Decreased expression of A20 may lead to an enhanced activation of proinflammatory Th17 cells, causing a reactivation of BD.

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