Differential Expression of Suppressor of Cytokine Signalling Proteins in Behçet's Disease

Hamedi, Mojgan; Bergmeier, Lesley A.; Hagi‐Pavli, Eleni; Vartoukian, Sonia R.; Fortune, Farida

doi:10.1111/sji.12211

Cited by 18 publications

(8 citation statements)

References 33 publications

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“…An increased expression of SOCS3, a regulator of the JAK/STAT pathway of cytokine induction, has been observed in all patients with BD irrespective of disease activity [ 61 ], and polymorphisms of HLA-DRB1 alleles have been associated with BD [ 62 ].…”

Section: Discussionmentioning

confidence: 99%

Gene Expression Profiling in Behcet’s Disease Indicates an Autoimmune Component in the Pathogenesis of the Disease and Opens New Avenues for Targeted Therapy

Puccetti

Fiore

Pelosi

et al. 2018

Journal of Immunology Research

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Behçet disease (BD) is a chronic inflammatory multisystem disease characterized by oral and genital ulcers, uveitis, and skin lesions. Disease etiopathogenesis is still unclear. We aim to elucidate some aspects of BD pathogenesis and to identify specific gene signatures in peripheral blood cells (PBCs) of patients with active disease using novel gene expression and network analysis. 179 genes were modulated in 10 PBCs of BD patients when compared to 10 healthy donors. Among differentially expressed genes the top enriched gene function was immune response, characterized by upregulation of Th17-related genes and type I interferon- (IFN-) inducible genes. Th17 polarization was confirmed by FACS analysis. The transcriptome identified gene classes (vascular damage, blood coagulation, and inflammation) involved in the pathogenesis of the typical features of BD. Following network analysis, the resulting interactome showed 5 highly connected regions (clusters) enriched in T and B cell activation pathways and 2 clusters enriched in type I IFN, JAK/STAT, and TLR signaling pathways, all implicated in autoimmune diseases. We report here the first combined analysis of the transcriptome and interactome in PBCs of BD patients in the active stage of disease. This approach generates useful insights in disease pathogenesis and suggests an autoimmune component in the origin of BD.

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Section: Discussionmentioning

confidence: 99%

Gene Expression Profiling in Behcet’s Disease Indicates an Autoimmune Component in the Pathogenesis of the Disease and Opens New Avenues for Targeted Therapy

Puccetti

Fiore

Pelosi

et al. 2018

Journal of Immunology Research

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“…This indicates the possibility that neutrophils with activated TLRs may provide additional stimulatory signals to γδ T cells thus establishing a strong interaction with each other. In addition suppressor of cytokine signalling (SOCS) proteins which negatively regulate the JAK-STAT signalling pathway of cytokine induction appears to be dysregulated in BD [ 55 ].…”

Section: Gamma Delta T Cells and Behçet's Diseasementioning

confidence: 99%

Gamma Delta (γδ) T Cells and Their Involvement in Behçet’s Disease

Hasan

Bergmeier

Petrushkin

et al. 2015

Journal of Immunology Research

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Behçet's disease (BD) is a multisystem inflammatory disorder characterized by orogenital ulcerations, ocular manifestations, arthritis, and vasculitis. The disease follows a relapsing-remitting course and its pathogenesis is unknown. Genetic predisposition and immune-dysregulation involving gamma delta (γδ) T cells are reported to have a role. γδ T cells are atypical T cells, which represent a small proportion of total lymphocytes. They have features of both innate and adaptive immunity and express characteristics of conventional T cells, natural killer cells, and myeloid antigen presenting cells. These unconventional T cells are found in the inflammatory BD lesions and have been suggested to be responsible for inducing and/or maintaining the proinflammatory environment characteristic of the disease. Over the last 20 years there has been much interest in the role of γδ T cells in BD. We review the literature and discuss the roles that γδ T cells may play in BD pathogenesis.

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“…Several other genes are of potential interest for enhancing the susceptibility for BD: CCR1, KLRC4, IL12A-ASN1, STAT4, MICA-A6, SOCS1, IL10 and IL23R-IL12RB2, IFI16, and AIM2, in addition to miRNA polymorphisms. [22][23][24][25][26][27][28] Regarding neurological involvement, the prevalence of HLA-B51/B5 among patients with NBD is not dissimilar to that found in patients with BD and without neurological signs.…”

Section: Behçet's Diseasementioning

confidence: 99%

Focus on neuro-Behçet's disease: A review

Caruso¹,

Moretti²

2018

Neurol India

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Behçet's disease (BD) is a multisystemic vasculitis disorder of almost unknown etiology, which involves small and large vessels and affects both veins and arteries. BD is characterized by recurrent oral aphthae (the main and most recurrent symptoms), genital ulcers, variable skin lesions, arthritis, uveitis, and thrombophlebitis. Other reported symptoms concern the involvement of the gastrointestinal and the central nervous system. Neuro-Behçet's disease (NBD) is one of the main causes of long-term morbidity and mortality, making its prompt recognition and treatment fundamental to attaining a better outcome. As pointed out by Kalra et al., there are definite consensus statements for BD, but less data are available for NBD. A multidisciplinary team of rheumatologists, dermatologists, ophthalmologists, neurologists, cardiovascular surgeons, and gastroenterologists, often led by rheumatologists, participate in the management of patients with BD and NBD.

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Differential Expression of Suppressor of Cytokine Signalling Proteins in Behçet's Disease

Cited by 18 publications

References 33 publications

Gene Expression Profiling in Behcet’s Disease Indicates an Autoimmune Component in the Pathogenesis of the Disease and Opens New Avenues for Targeted Therapy

Gene Expression Profiling in Behcet’s Disease Indicates an Autoimmune Component in the Pathogenesis of the Disease and Opens New Avenues for Targeted Therapy

Gamma Delta (γδ) T Cells and Their Involvement in Behçet’s Disease

Focus on neuro-Behçet's disease: A review

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