The association of novel IL-33 polymorphisms with sIL-33 and risk of systemic lupus erythematosus

Guo, Jing; Xiang, Yang; Peng, You‐Fan; Huang, Hua‐Tuo; Yan, Liang; Wei, Ye‐Sheng

doi:10.1016/j.molimm.2016.07.001

Cited by 35 publications

(33 citation statements)

References 28 publications

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“…IL-33 was demonstrated to positively correlate to acute-phase inflammatory markers such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), but no correlation to disease course was found [11]. A similar finding was reported by Guo et al, further supporting the crucial role of IL-33 in the early phase of SLE [16]. Therefore, given the considerable evidence pointing to the association of IL-33 in SLE, particularly during the early stage of the disease, it is necessary to further investigate its roles and mechanisms.…”

Section: Introductionsupporting

confidence: 67%

Early Treatment of Interleukin-33 can Attenuate Lupus Development in Young NZB/W F1 Mice

Jaya

Liu

Chan

2020

Cells

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Interleukin-33 (IL-33), a member of the IL-1 cytokine family, has been recently associated with the development of autoimmune diseases, including systemic lupus erythematosus (SLE). IL-33 is an alarmin and a pleiotropic cytokine that affects various types of immune cells via binding to its receptor, ST2. In this study, we determine the impact of intraperitoneal IL-33 treatments in young lupus, NZB/W F1 mice. Mice were treated from the age of 6 to 11 weeks. We then assessed the proteinuria level, renal damage, survival rate, and anti-dsDNA antibodies. The induction of regulatory B (Breg) cells, changes in the level of autoantibodies, and gene expression were also examined. In comparison to the control group, young NZB/W F1 mice administered with IL-33 had a better survival rate as well as reduced proteinuria level and lupus nephritis. IL-33 treatments significantly increased the level of IgM anti-dsDNA antibodies, IL-10 expressing Breg cells, and alternatively-induced M2 macrophage gene signatures. These results imply that IL-33 exhibits a regulatory role during lupus onset via the expansion of protective IgM anti-dsDNA as well as regulatory cells such as Breg cells and M2 macrophages.

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Section: Introductionsupporting

confidence: 67%

Early Treatment of Interleukin-33 can Attenuate Lupus Development in Young NZB/W F1 Mice

Jaya

Liu

Chan

2020

Cells

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“…However, they also suggested that, in order to clearly explore the detailed role of this gene on IL-33 expression and the susceptibility to SLE, further functional analysis and the independent case-control study within a large amount of samples from distinct ethnical populations requires to be further conducted, which may eliminate the bias of interaction effect on the current results. In terms of rs1891385, another finding based on 257 SLE patients and 283 healthy controls in the Chinese population showed that rs1891385A/C polymorphism of IL-33 was one of the critical factors affecting the risk of SLE [23]. Importantly, the rs1891385C allele resulted in the higher risk of SLE than rs1891385-A allele did.…”

Section: Discussionmentioning

confidence: 99%

Interaction between IL-33 Gene Polymorphisms and Current Smoking with Susceptibility to Systemic Lupus Erythematosus

Zhu

Xie

Qin

et al. 2019

Journal of Immunology Research

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Aims. This study is aimed at exploring the relation between IL-33 single-nucleotide polymorphisms (SNPs) and the risk of systemic lupus erythematosus (SLE). Methods. SNPStats (online software) was used to test the Hardy-Weinberg equilibrium in controls. Generalized multifactor dimensionality reduction (GMDR) was adopted to screen the preferable interaction between IL-33 SNPs and current smoking. Results. Logistic regression analysis based on the fundamental data of age, gender, BMI, current smoking, and alcohol drinking showed that both rs1929992-G and rs1891385-C alleles were correlated with an increasing risk of SLE, the ORs (95% CI) of which were 1.62 (1.21-2.05) and 1.64 (1.22-2.10), respectively. One two-locus model (rs1929992×current smoking) had a testing accuracy of 60.11% (P=0.0010). Through an overall multidimensional model, optimum cross-validation consistency was obtained. The analysis indicated that current smoking status influenced the SLE risk depending on the genotypes at rs1929992. Pairwise LD analysis indicated that haplotype rs1929992G-rs7044343T was statistically related to the elevating risk of SLE (P<0.05). Those subjects with the G-T haplotype had a higher SLE risk than those with other haplotypes, after correction with factors, including gender, alcohol drinking, age, BMI, and current smoking. Conclusions. The rs1929992-G and rs1891385-C allele, interaction between the rs1929992 gene and current smoking, and haplotype rs1929992G-rs7044343T were all risk factors of SLE.

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“…Recent studies found a positive correlation between the serum level of IL-33 and the onset of hepatitis B virus- (HBV-) related liver fibrosis, suggesting the possible involvement of IL-33 in the manifestation of chronic hepatitis [ 22 , 23 ]. Other studies suggest that increased IL-33 levels correlate with the acute-phase inflammatory response in autoimmune diseases such as systemic lupus erythematosus where the levels of serum IL-33 are positively correlated with the erythrocyte sedimentation rate (ESR) and C reactive protein (CRP) [ 24 , 25 ]. However, several animal studies have also demonstrated that IL-33 treatment can protect against septic shock and reduce inflammation in the lungs of mice infected with influenza virus [ 26 , 27 ].…”

Section: Discussionmentioning

confidence: 99%

Serum Levels of IL-33 and Correlation with IL-4, IL-17A, and Hypergammaglobulinemia in Patients with Autoimmune Hepatitis

Zhang

Yun

Yanbo

et al. 2018

Mediators of Inflammation

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This study investigated the role of IL-33 in the pathogenesis of autoimmune hepatitis (AIH). The levels of IL-33/sST2 and Th1/Th2/Th17-type cytokines were determined by enzyme-linked immunosorbent assay in serum samples obtained from 30 AIH patients and 20 healthy controls (HCs). In addition, a murine model of experimental AIH (EAIH) was established to investigate the role of IL-33 in disease progression. The serum levels of IL-33, sST2, Th17 cytokines (IL-17A), Th1 cytokines (IFN-γ, TNF-α), and Th2 cytokines (IL-4) were significantly elevated in AIH patients compared to HCs. Following immunosuppression therapy, serum levels of IL-33 and sST2 were significantly decreased. Additionally, the serum levels of IL-33 in AIH patients were correlated positively with markers of hypergammaglobulinemia (IgG, IgM, and IgA) and liver injury (γ-GT/ALP). Also, the serum levels of IL-33 in AIH patients were correlated positively with proinflammatory cytokine levels (IL-17A and IL-4). Interestingly, treatment of EAIH mice with a specific IL-33 neutralizing antibody significantly reversed the increasing trend in serum ALT/AST and inhibited the production of the type 2 (IL-4) and type 17 cytokines (IL-17) but not the type 1 cytokine (IFN-γ). Our findings highlight the possible role of the IL-33/sST2 axis in the progression of AIH, opening a new door for developing a novel therapeutic strategy for AIH.

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The association of novel IL-33 polymorphisms with sIL-33 and risk of systemic lupus erythematosus

Cited by 35 publications

References 28 publications

Early Treatment of Interleukin-33 can Attenuate Lupus Development in Young NZB/W F1 Mice

Early Treatment of Interleukin-33 can Attenuate Lupus Development in Young NZB/W F1 Mice

Interaction between IL-33 Gene Polymorphisms and Current Smoking with Susceptibility to Systemic Lupus Erythematosus

Serum Levels of IL-33 and Correlation with IL-4, IL-17A, and Hypergammaglobulinemia in Patients with Autoimmune Hepatitis

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