IL27 gene single nucleotide polymorphisms confer susceptibility to rheumatoid arthritis in Iranian population

Mohammadi, Sahar; Mansouri, Reza; Shahi, Abbas; Akhlaghi, Mehdi; Dashti, Navid; Aslani, Saeed; Mansouri, Mojtaba; Poursani, Shiva; Mahmoudi, Mahdi

doi:10.1016/j.mgene.2018.09.002

Cited by 7 publications

(5 citation statements)

References 13 publications

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“…In cases of incomplete treatment implementations, RA can result in joint harms and disability. The disease in heterogeneous and various clinical images and pathogenic pathways are seen (Almasi et al, ; Anaraki Mohammadi et al, ; Mahmoudi, Aslani, Fadaei, & Jamshidi, ; Malmström, Catrina, & Klareskog, ; Mohammadi et al, ; Mousavi et al, ; Shabgah, Navashenaq, Shabgah, Mohammadi, & Sahebkar, ).…”

Section: Introductionmentioning

confidence: 99%

Strategies toward rheumatoid arthritis therapy; the old and the new

Abbasi

Mousavi

Jamalzehi

et al. 2018

Journal Cellular Physiology

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295

181

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Currently, medications used to treat rheumatoid arthritis (RA) are glucocorticoids (GCs) and nonsteroidal anti‐inflammatory drugs (NSAIDs), predominantly used for controlling the pain and inflammation, disease‐modifying antirheumatic drugs (DMARDs), administered as first‐line medication for newly diagnosed RA cases, and biological therapies, used to target and inhibit specific molecules of the immune and inflammatory responses. NSAIDs and other GCs are effective in alleviating the pain, inflammation, and stiffness due to RA. DMARDs that are used for RA therapy are hydroxychloroquine, methotrexate, leflunomide, and sulfasalazine. The biological therapies, on the contrary, are chimeric anti‐CD20 monoclonal antibody, rituximab, inhibitors of tumor necrosis factor‐α (TNF‐α) like etanercept, infliximab, and adalimumab, a recombinant inhibitor of interleukin‐1 (IL‐1), anakinra, and costimulation blocker, abatacept. Moreover, newly under evaluation biological therapies include new TNF‐α inhibitors, JAK inhibitors, anti‐interleukin‐6‐receptor monoclonal antibodies (mABs), and antibodies against vital molecules involved in the survival and development of functional B cells. The new strategies to treat RA has improved the course of the disease and most of the patients are successful in remission of the clinical manifestations if the diagnosis of the disease occur early. The probability of remission increase if the diagnosis happens rapidly and treat‐to‐target approach are implemented. In this review article, we have attempted to go through the treatment strategies for RA therapy both the routine ones and those which have been developed over the past few years and currently under investigation.

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Section: Introductionmentioning

confidence: 99%

Strategies toward rheumatoid arthritis therapy; the old and the new

Abbasi

Mousavi

Jamalzehi

et al. 2018

Journal Cellular Physiology

Self Cite

295

181

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“…Associations with malignancies were found for the IL-27- T4730C polymorphism, which was linked to the susceptibility of developing colorectal, hepatocellular and esophageal neoplasms, but it was found protective for UC [ 44 , 48 ].…”

Section: Discussionmentioning

confidence: 99%

“…The IL-27- T4730C , IL-27- A964G and IL-23- R381Q polymorphisms were identified using polymerase chain reaction (PCR) and restriction fragment length polymorphism analysis (RFLP), according to the methods described by Mohamadi et al, Anber et al and Mosayebian et al [ 46 , 47 , 48 ].…”

Section: Methodsmentioning

confidence: 99%

Potential Contribution of IL-27 and IL-23 Gene Polymorphisms to Multiple Sclerosis Susceptibility: An Association Analysis at Genotype and Haplotype Level

Barac

Iancu

Văcăraș

et al. 2021

JCM

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(1) Background: interleukin 23 (IL-23) and interleukin 27 (IL-27) modulate the activity of T helper 17 cells (Th17) with critical roles in autoimmune diseases and multiple sclerosis (MS). The genes responsible for cytokine generation are highly influenced by the presence of single nucleotide polymorphisms (SNP) in main regions such as regulatory sequences or in promoter regions, contributing to disease susceptibility and evolution. The present study analyzed the associations of IL-23 and IL-27 SNPs with susceptibility to multiple sclerosis. (2) Methods: We performed a case-control study including 252 subjects: 157 patients diagnosed with MS and 95 controls. We used polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) to determine the genotypes for IL-27 T4730С (rs 181206), IL-27 A964G (rs 153109), and IL-23 receptor gene (IL-23R) G1142A (rs 11209026). (3) Results: The IL27-T4730С gene polymorphism was significantly associated with an increased odds of MS under the dominant genetic model (TC + CC variant genotypes, adjusted odds ratio OR = 4.06, 95% CI: 2.14–7.83, p-value = 0.000007, Q-value = 0.000063). Individuals carrying the IL-27 A924G variant (AG + GG) genotype presented higher odds of MS compared to non-carriers under the dominant model (adjusted OR = 1.93, 95% CI: 1.05–3.51, p-value = 0.0324, Q-value = 0.05832) and the allelic genetic model (unadjusted p-value = 0.015, OR = 1.58, 95% CI: 1.09–2.28), while IL-23-R381Q SNP conferred a decreased odds of MS under a codominant model of inheritance (adjusted OR = 0.26, 95% CI: 0.08–0.92, p-value = 0.0276, Q-value = 0.058) and an allelic model (unadjusted p-value = 0.008, OR = 0.23, 95% CI: 0.07–0.75). In an additive model with adjustment for age group (≤40 years vs. >40 years), sex and smoking, patients carrying the G-C (A964G, T4730C) haplotype had a 3.18 increased risk (95% CI: 1.74–5.81, p < 0.001) to develop multiple sclerosis. (4) Conclusions: The results of the current study showed a significant relationship of IL-27-A964G and IL-27-T4730C polymorphisms with increased risk of MS, and also the protective role of the IL-23-R381Q polymorphism. Moreover, the haplotype-based analysis proposed the mutant G-C (A924G, T4730C) as a significant risk haplotype for the development of MS.

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“…PCR-restriction fragment length polymorphism analysis for IL27-T4730C polymorphism. The IL27-T4730C polymorphism was identified using the method described by Anaraki Mohammad et al (16). Fast PCR amplification was performed in an iCycler C1000 BioRad (Bio-Rad Life Science, Hercules, CA, USA) under the following conditions: Initial denaturation at 95˚C for 0.6 s, followed by 34 cycles of denaturation at 95˚C for 0.3 s, annealing of the primers at 67˚C for 0.3 s, and a final extension at 72˚C for 0.3 s. The specificity of the amplification reaction was checked by electrophoresis of 10 μl PCR product on 2% agarose gel stained with 10 mg/ml ethidium bromide solution.…”

Section: Methodsmentioning

confidence: 99%

“…One of the polymorphisms associated with the IL27p28 gene, T4730C (rs181206), has been investigated in esophageal, hepatocellular and colorectal neoplasms and other autoimmune disorders: immune thrombocytopenia, systemic lupus erythematosus (SLE), RA, Behcet's disease and ulcerative colitis (15,16). T4730C (rs181206) is a polymorphism located in exon 4 of the IL27 gene, consisting of a single nucleotide substitution of T with C at nucleotide 4730, which determines the substitution of Leu with Pro in 119 position of IL27 (Leu119Pro) (17)(18)(19).…”

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confidence: 99%

IL27 T4730C Polymorphism and Serology in Multiple Sclerosis: A Pilot Study

Barac

Văcăraș

Cozma

et al. 2021

In Vivo

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Background: Multiple sclerosis (MS) is one of the most debilitating neurological diseases of young adults. The presence of a single nucleotide polymorphism in the promoter regions of the interleukin 27 gene (IL27 T4730C, rs181206) may alter the transcription and the production of cytokine levels, leading to MS. Patients and Methods: We performed a case-control study including 82 individuals: 51 patients diagnosed with MS and 31 healthy controls. Polymerase chain reaction-restriction fragment length polymorphism was used in order to determine the genotypes for the IL27 T4730С polymorphism and enzyme-linked immunosorbent assay to measure the serum IL27 level. Results: Carriers of the T4730С polymorphism were found to have a 6-fold [95% confidence intervaI (CI)=1.83-19.63, p=0.002] increased risk for MS. Univariate logistic regression analysis showed an increased frequency of the TC4730 heterozygous genotype (39.2% vs. 9.7%) and also of the C4730 allele (27.45% vs. 8.06) in patients compared to controls, with a 6.02-fold increased risk (95% CI=1.61-22.46, p=0.006) and a 4.31-fold increased risk (95% CI=1.57-11.87, p=0.002) of developing MS. IL27 levels were significantly lower in patients compared to controls (12.35 versus 14.34 pg/ml, p=0.039), without significant differences between genotypes. Multivariate logistic analysis showed that IL27 T4730C polymorphism (odds ratio=6.272, 95% CI=1.84-21.40, p=0.003) and smoking (odds ratio=4.214, 95% CI=1.39-12.74, p=0.011) represented independent risk factors for MS. Conclusion: Our study provides a possible link between IL27 level and IL27 T4730C gene polymorphism and the risk for developing MS in a Romanian population.Multiple sclerosis (MS) is a central nervous system autoimmune disease, characterized by chronic inflammation, myelin damage, oligodendrocyte death and axonal loss leading to neurodegeneration and neurological dysfunctions (1). The pathogenesis of MS is linked to the activation of Tlymphocytes, influenced by environmental and gene interactions (2). In MS, the genetic influence has been demonstrated by genome-wide association studies and familial studies, discovering more than 50 susceptibility loci that contribute to disease onset, such as the polymorphisms located on chromosome 6p21, expressing the human leukocyte antigen class II region of the major histocompatibility complex (MHC), and in other non-MHC loci located near or inside genes controlling the function of the adaptive immune system (3). The involvement of MHC polymorphisms in autoimmune diseases is still unclear but some studies suggested that the binding between T-cell recognition sites and the peptide cleft of MHC molecules might be one explanation, associated with a reduced population of T-regulatory cells and cross reactivity between infectious antigens and self-proteins (4-6). In this respect, 2845This article is freely accessible online.

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IL27 gene single nucleotide polymorphisms confer susceptibility to rheumatoid arthritis in Iranian population

Cited by 7 publications

References 13 publications

Strategies toward rheumatoid arthritis therapy; the old and the new

Strategies toward rheumatoid arthritis therapy; the old and the new

Potential Contribution of IL-27 and IL-23 Gene Polymorphisms to Multiple Sclerosis Susceptibility: An Association Analysis at Genotype and Haplotype Level

IL27 T4730C Polymorphism and Serology in Multiple Sclerosis: A Pilot Study

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