Interleukin-33 gene expression and rs1342326 polymorphism in Behçet’s disease

Talei, Mahsa; Abdi, Ahmad; Shanebandi, Dariush; Jadidi‐Niaragh, Farhad; Khabazi, Alireza; Babaie, Farhad; Alipour, Shahriar; Afkari, Babak; Sakhinia, Ebrahim; Babaloo, Zohreh

doi:10.1016/j.imlet.2018.11.005

Cited by 14 publications

(8 citation statements)

References 28 publications

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“…Among them, IL-1-related cytokines, thus including IL-33, have been recently studied. Indeed, Talei et al [16] demonstrated that a specific polymorphism of the IL-33 gene, the rs1342326 T/G, may explain genetic susceptibility to BD, highlighting that this polymorphism may up-regulate IL-33 expression. Notably, Çerçi et al [17] conducted a study to investigate the role of IL-33 among BD patients.…”

Section: Autoimmune Disordersmentioning

confidence: 99%

IL-33/IL-31 Axis in Immune-Mediated and Allergic Diseases

Murdaca

Greco

Tonacci

et al. 2019

IJMS

110

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Several allergic and immunologic diseases including asthma, food allergy (FA), chronic spontaneous urticaria (CSU), atopic dermatitis (AD), systemic lupus erythematosus (SLE), systemic sclerosis (SSc), rheumatoid arthritis (RA), and Behçet’s disease (BD) are characterized by the involvement of Th2 immunity. Several mediators lead to immunoglobulin (Ig)E production, thus including key cytokines such as interleukin (IL)-4, IL-5, and IL-13. Among them, IL-31 and IL-33 have been recently studied as novel biomarkers and future therapeutic targets for allergic and immunological disorders. IL-31 is a proinflammatory cytokine—it regulates cell proliferation and is involved in tissue remodeling. IL-33, acting through its receptor suppression of tumorigenity (ST2L), is an alarmin cytokine from the IL-1 family, whose expression is mediated by tissue damage. The latter has a pleiotropic effect, as it may modulate specific and innate immune cells functions. To date, several researchers have investigated the involvement of IL-31 and IL-33 in several allergic and immune-mediated diseases. Further studies are needed to understand the future applications of these molecules as novel therapeutic agents. This paper aims to give the readers a complete and updated review of IL-31 and IL-33 involvement among the most common autoimmune and allergic disorders.

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Section: Autoimmune Disordersmentioning

confidence: 99%

IL-33/IL-31 Axis in Immune-Mediated and Allergic Diseases

Murdaca

Greco

Tonacci

et al. 2019

IJMS

110

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“…By contrast, a consistent association between IL33 rs7025417 and GCA was found, pointing out this polymorphism as a novel genetic risk factor for GCA susceptibility 34 . In addition, the potential role of an IL33 polymorphism (rs1342326) in the pathogenesis of Behçet’s disease, a condition affecting blood vessels of all sizes and types 31 , was assessed in Iranians 36 . With this respect, an effect of this genetic variant in the susceptibility to this disease was disclosed 36 .…”

Section: Discussionmentioning

confidence: 99%

“…In addition, the potential role of an IL33 polymorphism (rs1342326) in the pathogenesis of Behçet’s disease, a condition affecting blood vessels of all sizes and types 31 , was assessed in Iranians 36 . With this respect, an effect of this genetic variant in the susceptibility to this disease was disclosed 36 .…”

Section: Discussionmentioning

confidence: 99%

Role of the IL33 and IL1RL1 pathway in the pathogenesis of Immunoglobulin A vasculitis

Prieto-Peña

Remuzgo‐Martínez

Genre

et al. 2021

Sci Rep

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Cytokines signalling pathway genes are crucial factors of the genetic network underlying the pathogenesis of Immunoglobulin-A vasculitis (IgAV), an inflammatory vascular condition. An influence of the interleukin (IL)33- IL1 receptor like (IL1RL)1 signalling pathway on the increased risk of several immune-mediated diseases has been described. Accordingly, we assessed whether the IL33-IL1RL1 pathway represents a novel genetic risk factor for IgAV. Three tag polymorphisms within IL33 (rs3939286, rs7025417 and rs7044343) and three within IL1RL1 (rs2310173, rs13015714 and rs2058660), that also were previously associated with several inflammatory diseases, were genotyped in 380 Caucasian IgAV patients and 845 matched healthy controls. No genotypes or alleles differences were observed between IgAV patients and controls when IL33 and IL1RL1 variants were analysed independently. Likewise, no statistically significant differences were found in IL33 or IL1RL1 genotype and allele frequencies when IgAV patients were stratified according to the age at disease onset or to the presence/absence of gastrointestinal (GI) or renal manifestations. Similar results were disclosed when IL33 and IL1RL1 haplotypes were compared between IgAV patients and controls and between IgAV patients stratified according to the clinical characteristics mentioned above. Our results suggest that the IL33-IL1RL1 signalling pathway does not contribute to the genetic network underlying IgAV.

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“…Serum and skin tissue of IL-33 and sST2 levels were reported to be elevated in patients with BD, and sST2 is associated with ESR and CRP ( 95 ). Another study reported that in BD patients of Iran, the expression of IL-33 mRNA in PBMCs was much higher than in healthy controls, and rs1342326 T/G polymorphism of the IL-33 gene might contribute to the genetic susceptibility to BD ( 96 ). These results suggest that IL-33 may play an important role in the pathogenesis of BD.…”

Section: Il-33/st2 Axis In Rheumatic Diseasesmentioning

confidence: 99%

IL-33 in Rheumatic Diseases

2021

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Interleukin-33 (IL-33) is a nuclear factor mainly expressed in barrier epithelium, endothelial cells, and fibroblast reticular cells. Some inflammatory cells also express IL-33 under certain conditions. The important role of IL-33 in allergic reactions, helminth infection, cancer, tissue fibrosis, chronic inflammation, organ transplantation, and rheumatic immune diseases has been extensively studied in recent years. IL-33 primarily activates various circulating and tissue-resident immune cells, including mast cell, group 2 innate lymphoid cell (ILC2), regulatory T cell (Treg), T helper 2 cell (Th2), natural killer cell (NK cell), and macrophage. Therefore, IL-33 plays an immunomodulatory role and shows pleiotropic activity in different immune microenvironments. The IL-33/serum stimulation-2 (ST2) axis has been shown to have a detrimental effect on rheumatoid arthritis, systemic lupus erythematosus, and other rheumatic diseases. Interestingly, IL-33 also plays a protective role in the repair of barrier epithelium and the activation of Tregs. Therefore, the role of IL-33/ST2 depends on the underlying pathological conditions in rheumatic diseases. This review focuses on the dual role of the IL-33/ST2 axis in rheumatic diseases.

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Interleukin-33 gene expression and rs1342326 polymorphism in Behçet’s disease

Cited by 14 publications

References 28 publications

IL-33/IL-31 Axis in Immune-Mediated and Allergic Diseases

IL-33/IL-31 Axis in Immune-Mediated and Allergic Diseases

Role of the IL33 and IL1RL1 pathway in the pathogenesis of Immunoglobulin A vasculitis

IL-33 in Rheumatic Diseases

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