Investigating the role of IL-33 in the pathogenesis of Behçet’s Disease

Çerçi, Pamir; İnal, Ali; Köse, Kenan; Keskin, Göksal; Ölmez, Ümit

doi:10.1080/17843286.2017.1314241

Cited by 17 publications

(9 citation statements)

References 23 publications

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“…By combining these 2 approaches, we identified 82 genes significantly modulated in DE compared to NE. Among those genes, a few are already known to be implicated in uveitis, such as E and P selectins [43], CD44 [44], IL-33 [45,46] and Lcn2 [47]. Other genes were already implicated in other inflammatory disease models but not in uveitis, such as Lrg1 [48], Ackr1 [49] and Timp1 [50].…”

Section: Discussionmentioning

confidence: 99%

Retinal endothelial cell phenotypic modifications during experimental autoimmune uveitis: a transcriptomic approach

et al. 2020

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Background: Blood-retinal barrier cells are known to exhibit a massive phenotypic change during experimental autoimmune uveitis (EAU) development. In an attempt to investigate the mechanisms of blood-retinal barrier (BRB) breakdown at a global level, we studied the gene regulation of total retinal cells and retinal endothelial cells during non-infectious uveitis. Methods: Retinal endothelial cells were isolated by flow cytometry either in Tie2-GFP mice (CD31 + CD45 − GFP + cells), or in wild type C57BL/6 mice (CD31 + CD45 − endoglin + cells). EAU was induced in C57BL/6 mice by adoptive transfer of IRBP1-20-specific T cells. Total retinal cells and retinal endothelial cells from naïve and EAU mice were sorted and their gene expression compared by RNA-Seq. Protein expression of selected genes was validated by immunofluorescence on retinal wholemounts and cryosections and by flow cytometry. Results: Retinal endothelial cell sorting in wild type C57BL/6 mice was validated by comparative transcriptome analysis with retinal endothelial cells sorted from Tie2-GFP mice, which express GFP under the control of the endothelial-specific receptor tyrosine kinase promoter Tie2. RNA-Seq analysis of total retinal cells mainly brought to light upregulation of genes involved in antigen presentation and T cell activation during EAU. Specific transcriptome analysis of retinal endothelial cells allowed us to identify 82 genes modulated in retinal endothelial cells during EAU development. Protein expression of 5 of those genes (serpina3n, lcn2, ackr1, lrg1 and lamc3) was validated at the level of inner BRB cells. Conclusion: Those data not only confirm the involvement of known pathogenic molecules but further provide a list of new candidate genes and pathways possibly implicated in inner BRB breakdown during non-infectious posterior uveitis.

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Section: Discussionmentioning

confidence: 99%

Retinal endothelial cell phenotypic modifications during experimental autoimmune uveitis: a transcriptomic approach

et al. 2020

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“…IL33 SNPs rs7044343 and rs11792633 have been studied in various diseases such as Behçet's disease,[4041] systemic sclerosis, and rheumatoid arthritis,[1042] whereas rs1157505 is associated with the risk of developing AD. [943] There have been no studies which probe into the association of IL-33 gene polymorphism with periodontal disease, in hitherto published literature.…”

Section: Discussionmentioning

confidence: 99%

Higher interleukin-33 levels in aggressive periodontitis cases

Ballambettu

Pradeep

Purushottam

et al. 2019

J Indian Soc Periodontol

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“…IL‐33, a new member of the IL‐1 family, is essential in regulating immune responses and inflammatory vascular disorders. A study by Çerçi et al () showed that the IL‐33 serum levels were significantly higher in BD patients compared with that the healthy controls. Furthermore, in active BD patients with arthritis, the serum IL‐33 levels were higher, but not significant, in the control group.…”

Section: Antigens Eliciting Autoantibody Responsesmentioning

confidence: 97%

Behçet’s disease: An immunogenetic perspective

Salmaninejad

Zamani

Shabgah

et al. 2018

Journal Cellular Physiology

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Behçet’s disease (BD) is a chronic and rare multisystemic disorder defined by autoimmunity and inflammatory characteristics, manifested by ocular lesions, recurrent genital and oral ulcers, skin symptoms and arthritis as well as neurological, intestinal, and vascular involvement. Despite the unknown cause of BD, there is some strong documentation for immunological, genetic, environmental, and infectious factors playing a role in the pathogenesis of BD. While the nature of the genetic variants remains unidentified, many genetic risk factors are considered to contribute to BD susceptibility. Along with human leukocyte antigen gene encoding B*51 (HLA‐B*51) and areas including the major histocompatibility complex class I, genome‐wide association studies have recognized numerous other BD susceptibility genes including those encoding interleukin (IL)‐10, IL‐12 receptor β 2 (IL‐12RB2), IL‐23 receptor (IL‐23R), C‐C chemokine receptor 1 gene, signal transducer and activator of transcription 4 (STAT4), endoplasmic reticulum aminopeptidase (ERAP1), and genes encoding killer cell lectin‐like receptor family members (KLRC4‐KLRK1). It is believed that BD could be considered as a disorder lying in between autoimmune and autoinflammatory syndromes. The positive responses to classical immunosuppressive agents like azathioprine and cyclosporine and involvement of autoantigens in the initiation of the disorder are the main BD features that reflect the autoimmune nature of the disorder. In this review, we address recent findings on the role of common cytokines, antibodies and immunogenetic factors in BD.

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Investigating the role of IL-33 in the pathogenesis of Behçet’s Disease

Abstract: IL-33 may play a significant role of in the pathogenesis of BD.

Cited by 17 publications

References 23 publications

Retinal endothelial cell phenotypic modifications during experimental autoimmune uveitis: a transcriptomic approach

Retinal endothelial cell phenotypic modifications during experimental autoimmune uveitis: a transcriptomic approach

Higher interleukin-33 levels in aggressive periodontitis cases

Behçet’s disease: An immunogenetic perspective

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