• Asian Pacific Journal of Cancer Prevention
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• 제15권20호
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• pp.8775-8778
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• 2014

Background: To explore the relationship between polymorphisms of interleukin17 (IL-17) gene(A-832G 7488A/G) and the susceptibility to silicosis, a risk factor for lung cancer. Materials and Methods: A total of 113 silicosis patients and 116 workers without silicosis were enrolled in the case-control study. IL-17A A-832G and IL-17F 7488A/G polymorphisms were evaluated by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Results: The frequencies of AA,GG and AG of IL-17A A-832G locus in the case and control groups were 46.9%, 8.0%, 45.1%, and 49.2%, 7.6%, 43.2%, respectively, with no significant differences (p>0.05).The GG genotype in the IL-17F (7488A/G) locus was not found. The frequencies of AA and GA of IL-17F 7488A/G locus in the case and control groups were 84.1%, 15.9% and 66.4%, 33.6%, respectively (p<0.05). Analysis of combined effects showed that the individuals with GG+AG genotype of IL-17A and GG+GA genotype of IL-17F are protected against silicosis (OR=0.469). Conclusions: IL-17F 7488A/G is associated with susceptibility to silicosis, and G allele may have a protective effect. No relationship was found between IL-17A gene polymorphisms at A-832G and silicosis.

• Asian Pacific Journal of Cancer Prevention
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• 제15권20호
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• pp.8709-8713
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• 2014

Background: Previous studies have indicated that single nucleotide polymorphisms (SNPs) of the interleukin-17 (IL-17) gene are associated with an increased risk of gastric cancer. However, the findings were inconsistent. Materials and Methods: To provide a more reliable estimation of the association between SNPs in the IL-17 gene and the susceptibility to gastric cancer, we searched PubMed, CNKI, and Wan Fang databases and selected finally six studies covering 2,366 cases and 3,205 controls to perform a meta-analysis. Results: Statistical analyses showed that an rs2275913 polymorphism within the IL-17A gene was significantly associated with an increased risk of gastric cancer using a generalized odds ratio (ORG, a model-free approach). Moreover, we also found that the 'A' allele carriers of IL-17A rs2275913 had a significant link with clinicopathological features. However, no significant positive signals were observed in the association analysis of the rs3748067 and rs763780 polymorphisms with the risk of gastric cancer in IL-17A and IL-17F, respectively. Conclusions: Despite some limitations, the present meta-analysis provided a more precise estimation of the relationship between the IL-17 gene SNPs and gastric cancer risk compared with individual studies.

• IMMUNE NETWORK
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• 제24권1호
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• pp.2.1-2.24
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• 2024

Studies over the last 2 decades have identified IL-17 and IL-21 as key cytokines in the modulation of a wide range of immune responses. IL-17 serves as a critical defender against bacterial and fungal pathogens, while maintaining symbiotic relationships with commensal microbiota. However, alterations in its levels can lead to chronic inflammation and autoimmunity. IL-21, on the other hand, bridges the adaptive and innate immune responses, and its imbalance is implicated in autoimmune diseases and cancer, highlighting its important role in both health and disease. Delving into the intricacies of these cytokines not only opens new avenues for understanding the immune system, but also promises innovative advances in the development of therapeutic strategies for numerous diseases. In this review, we will discuss an updated view of the immunobiology and therapeutic potential of IL-17 and IL-21.

• IMMUNE NETWORK
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• 제14권3호
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• pp.156-163
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• 2014

Interleukin (IL) 17 is produced by T-helper (Th) 17 with a vigorous effect on cells of the immune system playing important roles in pathogenesis of immune-mediated diseases, including autoimmune disorders and cancers. Therefore, the aim of current study was to determine the serum levels of IL-6, IL-17, and transforming growth factor beta (TGF-${\beta}$) in Iranian bladder cancer patients, and to correlate them with disease status. Blood samples were collected from 40 bladder cancer patients and 38 healthy individuals with no history of malignancies or autoimmune disorders. The serum levels of IL-6, IL-17, and TGF-${\beta}$ were measured by the enzyme-linked immunosorbent assay (ELISA). The results showed that the levels of IL-17 (p<0.0001) and TGF-${\beta}$ (p<0.0001) were significantly lower in the patients compared to the controls. No significant differences in the level of serum IL-6 (p=0.16) was observed between the patients and controls. In addition, demographic characteristics between control and patients groups were not significantly different. As most of the cases studied in this investigation were in stage I and II, it is concluded that reduced Th17-related cytokines can be used as indicators for following the course and clinical stages of bladder carcinoma progress and immune response to cancer.

• Clinical and Experimental Pediatrics
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• 제53권2호
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• pp.215-221
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• 2010

목 적 : IgA 신병증은 세계적으로 가장 흔한 사구체 질환으로 최근 들어 interleukin (IL)-17의 면역조절 반응에 있어서의 관련성이 밝혀지고 있다. 이 연구에서는 IL-17RA 유전자의 단일 염기다형성과 소아 IgA 신병증의 발생 및 진행과의 연관성을 알아보고자 하였다. 방 법 : 조직 검사를 통해 확인된 IgA 신병증 환아 156명과 건강한 정상 성인 245명을 대조군으로 하여 말초혈액을 채취하였다. PCR 방법으로 IL-17RA 유전자의 SNP (rs2895332, rs1468488, rs4819553)를 분석하였다. 환자군을 단백뇨(${\leq}4$ and >$4mg/m^2/hr$, ${\leq}40$ and >$40mg/m^2/hr$)와 병리학적 진행 여부에 따라서 두 그룹으로 나누어 IL-17RA SNP와의 연관성을 확인하였다. 결 과 : IgA 신병증 환자군과 정상 대조군에서 IL-17RA 유전자 rs2895332, rs1468488, rs4819553의 발현율은 통계적으로 유의한 차이가 없었다. 또한 IL-17RA 유전자 각각에 대하여, 병리학적 진행성 병변을 가진 군과 그렇지 못한 군 사이에 통계학적으로 유의한 차이가 없었다. 그러나 rs2895332 유전자의 경우, 단백뇨가 있는 군(단백뇨>$4mg/m^2/hr$)과 없는 군(단백뇨${\leq}4mg/m^2/hr$)에서는 두 군간에 통계적으로 유의한 차이를 보였다. 결 론 : IL-17RA 유전자 rs2895332의 단일염기다형성은 소아의 IgA 신병증에서 단백뇨의 발생과 통계학적으로 의미 있는 연관성이 있었다.

• Journal of Microbiology and Biotechnology
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• 제30권12호
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• pp.1810-1818
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• 2020

Inhibitor K562 (IK) protein was first isolated from the culture medium of K562 cells, a leukemia cell line, and is an inhibitory regulator of interferon-γ-induced major histocompatibility complex class II expression. Recently, exogenous truncated IK (tIK) protein showed potential as a therapeutic agent for inflammation-related diseases. In this study, we designed a novel putative anti-inflammatory peptide derived from tIK protein based on homology modeling of the human interleukin-10 (hIL-10) structure, and investigated whether the peptide exerted inhibitory effects against pro-inflammatory cytokines such as IL-17 and tumor necrosis factor-α (TNF-α). The peptide contains key residues involved in binding hIL-10 to the IL-10 receptor, and exerted strong inhibitory effects on IL-17 (43.8%) and TNF-α (50.7%). In addition, we used circular dichroism spectroscopy to confirm that the peptide is usually present in a random coil configuration in aqueous solution. In terms of toxicity, the peptide was found to be biologically safe. The mechanisms by which the short peptide derived from human tIK protein exerts inhibitory effects against IL-17 and TNF-α should be explored further. We also evaluated the feasibility of using this novel peptide in skincare products.

• Molecules and Cells
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• 제19권2호
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• pp.180-184
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• 2005

IL-17 is a major proinflammatory cytokine secreted by activated T-lymphocytes that accumulates in the inflamed joints of rheumatoid arthritis (RA) patients. Additional IL-17-related molecules and their receptors have been discovered and may also contribute to RA pathogenesis. We examined the expression of the prototypic IL-17 (IL-17A) and its homologs, IL-17B-F, by RT-PCR analyses of synovial fluid mononuclear cells (SFMCs) and peripheral blood mononuclear cells (PBMCs) from RA patients. We also tested for induction of the IL-17 receptor homologs upon stimulation of the fibroblast-like synoviocytes (FLSs) of RA patients with IL-17. The patients' SFMCs expressed IL-17C, E and F in addition to IL-17A. As in the case of IL-17, IL-15 appears to be the major inducer of these homologs in RA SFMCs. We detected transcripts of IL-17R, as well as those of IL-17RB, C and D, in the FLSs of RA patients. Whereas IL-17R expression increased upon in vitro stimulation with IL-17, expression of IL-17RB, C and D was unchanged. However the possibility of cross-interaction between other IL-17 homologs and receptor isoforms remains to be investigated. Our data suggest that these additional homologs should also be considered as targets for immune modulation in the treatment of RA joint inflammation.

• Molecules and Cells
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• 제39권7호
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• pp.536-542
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• 2016

Interleukin-17A is a member of the IL-17 family, and is known as CTLA8 in the mouse. It is produced by T lymphocytes and NK cells and has proinflammatory roles, inducing cytokine and chemokine production. However, its role in tumor biology remains controversial. We investigated the effects of locally produced IL-17A by transferring the gene encoding it into CT26 colon cancer cells, either in a secretory or a membrane-bound form. Expression of the membrane-bound form on CT26 cells dramatically enhanced their proliferation in vitro. The enhanced growth was shown to be due to an increased rate of cell cycle progression: after synchronizing cells by adding and withdrawing colcemid, the rate of cell cycle progression in the cells expressing the membrane-bound form of IL-17A was much faster than that of the control cells. Both secretory and membrane-bound IL-17A induced the expression of Sca-1 in the cancer cells. When tumor clones were grafted into syngeneic BALB/c mice, the tumor clones expressing the membrane-bound form IL-17A grew rapidly; those expressing the secretory form also grew faster than the wild type CT26 cells, but slower than the clones expressing the membrane-bound form. These results indicate that IL-17A promotes tumorigenicity by enhancing cell cycle progression. This finding should be considered in treating tumors and immune-related diseases.

• 한국콘텐츠학회:학술대회논문집
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• 한국콘텐츠학회 2018년도 춘계 종합학술대회 논문집
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• pp.551-552
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• 2018

K/BxN serum can induce arthritis in normal mice because of abundant autoantibodies that trigger an innate inflammatory response in joints. To determine whether IL-17 is involved in the pathogenesis of serum-induced arthritis, we injected wild-type and $IL-17^{-/-}$ mice with K/BxN serum and evaluated them for signs of arthritis. Unlike wild-type mice, $IL-17^{-/-}$ mice did not show any signs of arthritis. IL-17 was produced predominantly by $CD3^-CD4^-gdTCR^-NK1.1^-Sca1^{int}Thy1^{hi}$ cells residing in the inflamed synovial tissue. When synovial cells extracted from normal joints were stimulated with IL-23 or autoantibody-containing immune complexes, a substantial fraction of $Sca1^{int}Thy1^{hi}$ cells produced IL-17. Thus, we have identified a novel population of IL-17-producing innate synovial cells that play a crucial role in the development of K/BxN serum-induced arthritis.

• 한국임상수의학회지
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• 제17권2호
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• pp.311-315
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• 2000

Recombinant interleukin-2 (IL-2) has been demonstated as an antineoplastic agent in mice and human, and the route of administration is important to IL-2-induced therapeutic responses. Therefore, the current experiment was undertaken to clarify the effect of IL-2 administration route on antitumor response against subcutaneous Meth-A tumor in mice. At the beginning of each experiment, normal BALB/c mice were injected subcutaneously with $5{\times}10^6$ Meth-A tumor cells. Beginning on day 7, experimental groups were treated with a 5-day course of IL-2 (intraperitoneal or subcutaneous injection of 30, 000 IU every 12 hours for 5 days). The result of this experiment revealed that Meth-A tumor grew progressively in control mice. Intraperitoneal IL-2 treatment decreased significantly tumor growth and prolonged survival, compared with control mice. Subcutaneous IL-2 treatment decreased significantly tumor growth until day 11 and tumor cells, grew progressively thereafter, but mice in this group survived longer than control mice.