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

Zhu, Xiao‐Dong; Xie, Lin; Qin, Haihong; Liang, Jun; Yang, Yue; Xu, Jinhua; Zhang, Tiejun

doi:10.1155/2019/1547578

Cited by 23 publications

(20 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Genetic studies regarding IL-33 gene and its polymorphisms have also been conducted. Indeed, Zhu et al [28] analyzed two IL-33 single nucleotide polymorphisms (SNPs), demonstrating that both were potential risk factors for developing SLE. On the other hand, at least two studies reported different results.…”

Section: Autoimmune Disordersmentioning

confidence: 99%

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

Murdaca

Greco

Tonacci

et al. 2019

IJMS

119

View full text Add to dashboard Cite

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.

show abstract

Section: Autoimmune Disordersmentioning

confidence: 99%

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

Murdaca

Greco

Tonacci

et al. 2019

IJMS

119

View full text Add to dashboard Cite

show abstract

“…Previous studies have shown that rs1929992 was associated with the risk of several autoimmune diseases. Since it is functional and has not reported its relationship to HCC, we studied whether it is associated with HCC risk [ 36 – 38 ]. However, the results showed that the difference in distribution frequency of rs1929992 locus alleles and genotypes in the HCC case group and control group was not statistically significant ( p > 0.05), which was similar to the findings of Jafarzadeh et al in breast cancer [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

CD44, IL-33, and ST2 Gene Polymorphisms on Hepatocellular Carcinoma Susceptibility in the Chinese Population

Pan

Huang

et al. 2020

BioMed Research International

View full text Add to dashboard Cite

The interleukin- (IL-) 33/ST2 axis plays a pivotal role in tumorigenesis through influencing cancer stemness and other mechanisms. CD44 is one of the critical markers of hepatocellular carcinoma (HCC) among the cancer stem cells (CSCs). There is still a lack of CD44 gene single-nucleotide polymorphisms (SNPs) combined with IL-33/ST2 pathway single-nucleotide polymorphisms in HCC susceptibility analysis literature, although CD44 and IL-33/ST2 have been reported separately in human cancers. This study is aimed at investigating the relationship between CD44, IL-33, and ST2 SNPs and HCC susceptibility and clinicopathological features. We analyzed 565 HCC patients and 561 healthy controls in the Chinese population. The genes for CD44rs187115A>G, IL-33 rs1929992A>G, and ST2 rs3821204G>C were typed using the SNaPshot method. We found that the distribution frequencies of CD44 and ST2 alleles and genotypes in both the HCC case group and the control group were statistically significant ( p < 0.05 ). The results showed that individuals carrying at least one G allele of the CD44 rs187115 gene were at a higher risk than the AA genotype carriers ( p = 0.007 , odds ratio OR = 1.429 , 95% confidence interval (CI): 1.102–1.854). Similarly, individuals with at least one C allele of ST2 rs3821204 had a higher risk of HCC than those with GG genes ( p ≤ 0.001 , OR = 1.647 , 95% CI: 1.296-2.093). Combining the haplotype analysis of the 3 loci suggested that CD44 rs187115, IL-33 rs1929992, and ST2 rs3821204 are associated with the risk of HCC and could potentially serve as useful genetic markers for HCC in some populations of China.

show abstract

“…Moreover, a greater level of serum IL-33 was reported in Chinese SLE patients as compared to healthy individuals, albeit lower than in patients with RA [11]. Additionally, a case-study performed in the Chinese population reported an association between IL-33 polymorphism and susceptibility to SLE [14,15]. In contrast, a contradictory finding has been reported by Mok et al in which the serum level of IL-33 in SLE patients was not correlated to disease severity [12].…”

Section: Introductionmentioning

confidence: 91%

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

Jaya

Liu

Chan

2020

Cells

View full text Add to dashboard Cite

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.

show abstract

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

Cited by 23 publications

References 26 publications

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

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

CD44, IL-33, and ST2 Gene Polymorphisms on Hepatocellular Carcinoma Susceptibility in the Chinese Population

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

Contact Info

Product

Resources

About