Journal articles: 'Interleukin 37'

1

Dinarello, Charles A., and Philip Bufler. "Interleukin-37." Seminars in Immunology 25, no. 6 (December 2013): 466–68. http://dx.doi.org/10.1016/j.smim.2013.10.004.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Kaabachi, Wajih, Olfa Kacem, Rafik Belhaj, Agnes Hamzaoui, and Kamel Hamzaoui. "Interleukin-37 in endometriosis." Immunology Letters 185 (May 2017): 52–55. http://dx.doi.org/10.1016/j.imlet.2017.03.012.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

XU, JianYong, Zhong HUANG, LingYun LI, and Jing DU. "Interleukin-37 and autoimmune diseases." SCIENTIA SINICA Vitae 48, no. 1 (January 1, 2018): 30–39. http://dx.doi.org/10.1360/n052017-00228.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Özgüçlü, Selcan, Türker Duman, Funda Seher Özalp Ateş, Orhan Küçükşahin, Sevgi Çolak, and Ümit Ölmez. "Serum interleukin-37 level and interleukin-37 gene polymorphism in patients with Behçet disease." Clinical Rheumatology 38, no. 2 (September 18, 2018): 495–502. http://dx.doi.org/10.1007/s10067-018-4288-7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Xu, Wang-Dong, and An-Fang Huang. "Letter to Editor: Serum interleukin-37 level and interleukin-37 gene polymorphism in patients with Behçet disease." Clinical Rheumatology 38, no. 7 (May 20, 2019): 2017–18. http://dx.doi.org/10.1007/s10067-019-04599-x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

McNamee, E. N., J. C. Masterson, P. Jedlicka, M. McManus, A. Grenz, C. B. Collins, M. F. Nold, et al. "Interleukin 37 expression protects mice from colitis." Proceedings of the National Academy of Sciences 108, no. 40 (August 22, 2011): 16711–16. http://dx.doi.org/10.1073/pnas.1111982108.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Boisvert, W., S. McCurdy, and Y. Baumer. "Macrophage expression of interleukin-37 attenuates atherosclerosis." Atherosclerosis 275 (August 2018): e44. http://dx.doi.org/10.1016/j.atherosclerosis.2018.06.111.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Li, Weidong, Shijie Li, Xianjin Li, Shuzhong Jiang, and Bing Han. "Interleukin-37 elevation in patients with atrial fibrillation." Clinical Cardiology 40, no. 2 (November 2, 2016): 66–72. http://dx.doi.org/10.1002/clc.22630.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Pastorelli, Luca, and Theresa T. Pizarro. "Interleukin-37: A Peacekeeper at the Intestinal Borders." Digestive Diseases and Sciences 62, no. 5 (March 13, 2017): 1103–6. http://dx.doi.org/10.1007/s10620-017-4523-0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Alqazlan, Nadiyah, Hong Diao, Anthony M. Jevnikar, and Shengwu Ma. "Production of functional human interleukin 37 using plants." Plant Cell Reports 38, no. 3 (January 18, 2019): 391–401. http://dx.doi.org/10.1007/s00299-019-02377-2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Song, Lijun, Feng Qiu, Yuchen Fan, Feng Ding, Huaxiang Liu, Qiang Shu, Weiwei Liu, and Xingfu Li. "Glucocorticoid Regulates Interleukin-37 in Systemic Lupus Erythematosus." Journal of Clinical Immunology 33, no. 1 (September 9, 2012): 111–17. http://dx.doi.org/10.1007/s10875-012-9791-z.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Yan, Peng, Yuankai Zhang, Chunxiao Wang, Fang Lv, and Lijun Song. "Interleukin-37 (IL-37) Suppresses Pertussis Toxin-Induced Inflammatory Myopathy in a Rat Model." Medical Science Monitor 24 (December 18, 2018): 9187–95. http://dx.doi.org/10.12659/msm.910904.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

&NA;. "Interleukin-4-38-37-PE38KDEL gains orphan drug status." Inpharma Weekly &NA;, no. 1643 (June 2008): 22. http://dx.doi.org/10.2165/00128413-200816430-00061.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Allam, Gamal, Asmaa M. Gaber, Sarah I. Othman, and Adel Abdel-Moneim. "The potential role of interleukin-37 in infectious diseases." International Reviews of Immunology 39, no. 1 (October 21, 2019): 3–10. http://dx.doi.org/10.1080/08830185.2019.1677644.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Zhang, Jun-Ai, Gan-Bin Liu, Bi-Ying Zheng, Yuan-Bin Lu, Yu-Chi Gao, Xiao-Zhen Cai, You-Chao Dai, et al. "Tuberculosis-sensitized monocytes sustain immune response of interleukin-37." Molecular Immunology 79 (November 2016): 14–21. http://dx.doi.org/10.1016/j.molimm.2016.09.018.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Ellisdon, Andrew M., Claudia A. Nold-Petry, Laura D’Andrea, Steven X. Cho, Jason C. Lao, Ina Rudloff, Devi Ngo, et al. "Homodimerization attenuates the anti-inflammatory activity of interleukin-37." Science Immunology 2, no. 8 (February 10, 2017): eaaj1548. http://dx.doi.org/10.1126/sciimmunol.aaj1548.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Tang, Ruohui, Jin Yi, Jing Yang, Yueqi Chen, Wei Luo, Shiwu Dong, and Jun Fei. "Interleukin-37 inhibits osteoclastogenesis and alleviates inflammatory bone destruction." Journal of Cellular Physiology 234, no. 5 (November 10, 2018): 7645–58. http://dx.doi.org/10.1002/jcp.27526.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Wu, B., K. Meng, Q. Ji, M. Cheng, K. Yu, X. Zhao, H. Tony, et al. "Interleukin-37 ameliorates myocardial ischaemia/reperfusion injury in mice." Clinical & Experimental Immunology 176, no. 3 (April 24, 2014): 438–51. http://dx.doi.org/10.1111/cei.12284.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Tawfik, Marwa G., Samah I. Nasef, Hanan H. Omar, and Mona S. Ghaly. "Serum Interleukin-37: a new player in Lupus Nephritis?" International Journal of Rheumatic Diseases 20, no. 8 (June 19, 2017): 996–1001. http://dx.doi.org/10.1111/1756-185x.13122.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Fujita, Hiroyuki, Yusuke Inoue, Katsuya Seto, Noriko Komitsu, and Michiko Aihara. "Interleukin-37 is elevated in subjects with atopic dermatitis." Journal of Dermatological Science 69, no. 2 (February 2013): 173–75. http://dx.doi.org/10.1016/j.jdermsci.2012.11.001.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Dinarello, Charles A., Claudia Nold-Petry, Marcel Nold, Mayumi Fujita, Suzhao Li, Soohyun Kim, and Philip Bufler. "Suppression of innate inflammation and immunity by interleukin-37." European Journal of Immunology 46, no. 5 (May 2016): 1067–81. http://dx.doi.org/10.1002/eji.201545828.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Zhuang, Xinyu, Bangwei Wu, Jian Li, Haiming Shi, Bo Jin, and Xinping Luo. "The emerging role of interleukin-37 in cardiovascular diseases." Immunity, Inflammation and Disease 5, no. 3 (May 26, 2017): 373–79. http://dx.doi.org/10.1002/iid3.159.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Nam, Seoung Wan, SuMan Kang, Jun Hyeok Lee, and Dae Hyun Yoo. "Different Features of Interleukin-37 and Interleukin-18 as Disease Activity Markers of Adult-Onset Still’s Disease." Journal of Clinical Medicine 10, no. 5 (February 26, 2021): 910. http://dx.doi.org/10.3390/jcm10050910.

Full text

Abstract:

The aim of this study was to evaluate the usefulness of serum interleukin (IL)-37 and IL-18 as disease activity markers of adult-onset Still’s disease (AOSD) and to compare their related clinical features. Forty-five patients with a set of high and subsequent low disease activity status of AOSD were enrolled. Modified Pouchot (mPouchot) score and serologic disease activity markers including levels of IL-37 and IL-18 were compared between high and low disease activity status. The relationships between disease activity parameters and differences in levels of cytokines according to each disease manifestation were evaluated in high disease activity status. mPouchot score and all disease activity markers including IL-37 and IL-18 significantly declined after treatment. Though both cytokines positively correlated with mPouchot score, the two did not correlate with each other in high disease activity status. IL-18 positively correlated with ferritin, AST, and LDH while IL-37 correlated better with CRP. The expression level of IL-37 was related to leukocytosis while IL-18 was related to pleuritis, pneumonitis, abnormal LFT, and hyperferritinemia. In addition, patients in the IL-18 dominant group presented with higher LDH levels and required a higher mean corticosteroid dose. In conclusion, IL-37 and IL-18 are disease activity markers reflecting different aspects of AOSD that can complement each other.

APA, Harvard, Vancouver, ISO, and other styles

24

Jia, Hailin, Jing Liu, and Bo Han. "Reviews of Interleukin-37: Functions, Receptors, and Roles in Diseases." BioMed Research International 2018 (2018): 1–14. http://dx.doi.org/10.1155/2018/3058640.

Full text

Abstract:

Interleukin-37 (IL-37) is an IL-1 family cytokine discovered in recent years and has 5 different isoforms. As an immunosuppressive factor, IL-37 can suppress excessive immune response. IL-37 plays a role in protecting the body against endotoxin shock, ischemia-reperfusion injury, autoimmune diseases, and cardiovascular diseases. In addition, IL-37 has a potential antitumor effect. IL-37 and its receptors may serve as novel targets for the study, diagnosis, and treatment of immune-related diseases and tumors.

APA, Harvard, Vancouver, ISO, and other styles

25

Ruggeri, R. M., M. Cristani, T. M. Vicchio, A. Alibrandi, S. Giovinazzo, A. Saija, A. Campennì, F. Trimarchi, and S. Gangemi. "Increased serum interleukin-37 (IL-37) levels correlate with oxidative stress parameters in Hashimoto’s thyroiditis." Journal of Endocrinological Investigation 42, no. 2 (May 23, 2018): 199–205. http://dx.doi.org/10.1007/s40618-018-0903-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Bello, Ramatu, Voon Chin, Mohammad Abd Rachman Isnadi, Roslaini Abd Majid, Maizaton Atmadini Abdullah, Tze Lee, Zainul Amiruddin Zakaria, Mohd Hussain, and Rusliza Basir. "The Role, Involvement and Function(s) of Interleukin-35 and Interleukin-37 in Disease Pathogenesis." International Journal of Molecular Sciences 19, no. 4 (April 11, 2018): 1149. http://dx.doi.org/10.3390/ijms19041149.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Jiang, Jianfa, Zhaoying Jiang, and Min Xue. "Serum and peritoneal fluid levels of interleukin-6 and interleukin-37 as biomarkers for endometriosis." Gynecological Endocrinology 35, no. 7 (January 11, 2019): 571–75. http://dx.doi.org/10.1080/09513590.2018.1554034.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Eisenmesser, Elan Z., Adrian Gottschlich, Jasmina S. Redzic, Natasia Paukovich, Jay C. Nix, Tania Azam, Lingdi Zhang, et al. "Interleukin-37 monomer is the active form for reducing innate immunity." Proceedings of the National Academy of Sciences 116, no. 12 (February 28, 2019): 5514–22. http://dx.doi.org/10.1073/pnas.1819672116.

Full text

Abstract:

Interleukin-37 (IL-37), a member of the IL-1 family of cytokines, is a fundamental suppressor of innate and acquired immunities. Here, we used an integrative approach that combines biophysical, biochemical, and biological studies to elucidate the unique characteristics of IL-37. Our studies reveal that single amino acid mutations at the IL-37 dimer interface that result in the stable formation of IL-37 monomers also remain monomeric at high micromolar concentrations and that these monomeric IL-37 forms comprise higher antiinflammatory activities than native IL-37 on multiple cell types. We find that, because native IL-37 forms dimers with nanomolar affinity, higher IL-37 only weakly suppresses downstream markers of inflammation whereas lower concentrations are more effective. We further show that IL-37 is a heparin binding protein that modulates this self-association and that the IL-37 dimers must block the activity of the IL-37 monomer. Specifically, native IL-37 at 2.5 nM reduces lipopolysaccharide (LPS)-induced vascular cell adhesion molecule (VCAM) protein levels by ∼50%, whereas the monomeric D73K mutant reduced VCAM by 90% at the same concentration. Compared with other members of the IL-1 family, both the N and the C termini of IL-37 are extended, and we show they are disordered in the context of the free protein. Furthermore, the presence of, at least, one of these extended termini is required for IL-37 suppressive activity. Based on these structural and biological studies, we present a model of IL-37 interactions that accounts for its mechanism in suppressing innate inflammation.

APA, Harvard, Vancouver, ISO, and other styles

29

Kang, Bin, Shimeng Cheng, Jinbiao Peng, Jingjing Yan, and Shuye Zhang. "Interleukin-37 gene variants segregated anciently coexist during hominid evolution." European Journal of Human Genetics 23, no. 10 (January 28, 2015): 1392–98. http://dx.doi.org/10.1038/ejhg.2014.302.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Wu, G.-C., H.-M. Li, J.-B. Wang, R.-X. Leng, D.-G. Wang, and D.-Q. Ye. "Elevated plasma interleukin-37 levels in systemic lupus erythematosus patients." Lupus 25, no. 12 (July 11, 2016): 1377–80. http://dx.doi.org/10.1177/0961203316646462.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Yuan, Zhi-Chao, Jia-Min Wang, An-Fang Huang, Lin-Chong Su, Shuang-Jing Li, and Wang-Dong Xu. "Elevated expression of interleukin-37 in patients with rheumatoid arthritis." International Journal of Rheumatic Diseases 22, no. 6 (March 6, 2019): 1123–29. http://dx.doi.org/10.1111/1756-185x.13539.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Zhu, Jifeng, Chuanjiang Xie, Hongjiu Qiu, and Ling Shi. "Correlation Between Level of Interleukin-37 and Rheumatoid Arthritis Progression." International Journal of General Medicine Volume 14 (May 2021): 1905–10. http://dx.doi.org/10.2147/ijgm.s309436.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Tsai, Ya-Chu, and Tsen-Fang Tsai. "Anti-interleukin and interleukin therapies for psoriasis: current evidence and clinical usefulness." Therapeutic Advances in Musculoskeletal Disease 9, no. 11 (November 2017): 277–94. http://dx.doi.org/10.1177/1759720x17735756.

Full text

Abstract:

Anti-interleukin (IL) therapies have emerged as a major treatment for patients with moderate-to-severe psoriasis. This article reviews the up-to-date results of pivotal clinical trials targeting the interleukins used for the treatment of psoriasis, including IL-1, IL-2, IL-6, IL-8, IL-10, IL-12, IL-17, IL-20, IL-22, IL-23, IL-36 and bispecific biologics IL-17A/tumor necrosis factor alpha (TNF-α). Cytokines involved in the circuits of psoriasis inflammation without ongoing clinical trials are also mentioned (IL-9, IL-13, IL-15, IL-16, IL-18, IL-19, IL-21, IL-24, IL-27, IL-33, IL-35, IL-37, and IL-38).

APA, Harvard, Vancouver, ISO, and other styles

34

Li, Suzhao, Jesus Amo-Aparicio, Charles P. Neff, Isak W. Tengesdal, Tania Azam, Brent E. Palmer, Rubèn López-Vales, Philip Bufler, and Charles A. Dinarello. "Role for nuclear interleukin-37 in the suppression of innate immunity." Proceedings of the National Academy of Sciences 116, no. 10 (February 21, 2019): 4456–61. http://dx.doi.org/10.1073/pnas.1821111116.

Full text

Abstract:

The IL-1 family member IL-37 broadly suppresses innate inflammation and acquired immunity. Similar to IL-1α and IL-33, IL-37 is a dual-function cytokine in that IL-37 translocates to the nucleus but also transmits a signal via surface membrane receptors. The role of nuclear IL-37 remains unknown on the ability of this cytokine to inhibit innate inflammation. Here, we compared suppression of innate inflammation in transgenic mice expressing native human IL-37 (IL-37Tg) with those of transgenic mice carrying the mutation of aspartic acid (D) to alanine (A) at amino acid 20 (IL-37D20ATg). The mutation D20A prevents cleavage of caspase-1, a step required for IL-37 nuclear translocation. In vitro, peritoneal macrophages from IL-37Tg mice reduced LPS-induced IL-1β, IL-6, TNFα and IFNγ by 40–50% whereas in macrophages from IL-37D20ATg mice this suppression was not observed, consistent with loss of nuclear function. Compared with macrophages from IL-37Tg mice, significantly less or no suppression of LPS-induced MAP kinase and NFκB activation was also observed in macrophages from IL-37D20ATg mice. In vivo, levels of IL-1β, IL-6, and TNFα in the lungs and liver were markedly reduced during endotoxemia in IL-37Tg mice but not observed in IL-37D20ATg mice. However, suppression of innate inflammation remains intact in the IL-37D20A mice once the cytokine is released from the cell and binds to its receptor. These studies reveal a nuclear function for suppression of innate inflammation and are consistent with the dual function of IL-37 and a role for caspase-1 in limiting inflammation.

APA, Harvard, Vancouver, ISO, and other styles

35

Li, Xia, Dianxuan Guo, Ying Chen, Youdong Hu, and Fenglin Zhang. "Effects of Altered Levels of Pro- and Anti-Inflammatory Mediators on Locations of In-Stent Reocclusions in Elderly Patients." Mediators of Inflammation 2020 (September 23, 2020): 1–12. http://dx.doi.org/10.1155/2020/1719279.

Full text

Abstract:

Imbalances of proatherogenic inflammatory and antiatherogenic inflammatory mediators were involved in the pathogenesis of atherosclerosis. This study sought to investigate the effects of proatherogenic inflammatory and antiatherogenic inflammatory mediators on the proximal, middle, and distal coronary artery reocclusions in elderly patients after coronary stent implantations. We measured the expression levels of proatherogenic inflammatory/antiatherogenic inflammatory cytokines. This included interleukin-1 β (IL-1 β), interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), high-sensitivity C-reactive protein (hs-CRP), interleukin-10 (IL-10), interleukin-17 (IL-17), interleukin-13 (IL-13), and interleukin-37 (IL-37) in the elderly patients with the proximal, middle, and distal coronary artery reocclusions after coronary stent implantations. Levels of IL-1 β, IL-6, IL-8, TNF-α, and hs-CRP were remarkably increased (P<0.001), and levels of IL-10, IL-17, IL-13, and IL-37 were remarkably lowered (P<0.001) in the elderly patients with the proximal, middle, and distal coronary artery reocclusions. Imbalances of proatherogenic inflammatory and antiatherogenic inflammatory mediators may be involved in the formation and progression of proximal, middle, and distal coronary artery reocclusions in elderly patients after coronary stent implantations.

APA, Harvard, Vancouver, ISO, and other styles

36

Shilovskiy, I. P., M. E. Dyneva, O. M. Kurbacheva, D. A. Kudlay, and M. R. Khaitov. "The Role of Interleukin-37 in the Pathogenesis of Allergic Diseases." Acta Naturae 11, no. 4 (December 15, 2019): 54–64. http://dx.doi.org/10.32607/20758251-2019-11-4-54-64.

Full text

Abstract:

Cytokines of the interleukin-1 (IL-1) family play an important role in the realization of the protective functions of innate immunity and are the key mediators involved in the pathogenesis of a wide range of diseases, including various manifestations of allergy. The IL-1 family includes more than 11 members. However, the functions of many of them remain to be elucidated. Recently, new members of the IL-1 family have been discovered. In 2000, several independent research groups reported the discovery of a new interleukin of this family, which was named IL-37, or IL-1F7 (according to the new nomenclature). IL-37 was assigned to the IL-1 family based on its structural similarity with other members of this family. The study of its biological properties showed that its activity changes in inflammatory diseases, such as rheumatoid arthritis, psoriasis, as well as allergic diseases (allergic rhinitis, bronchial asthma, and atopic dermatitis). However, unlike most members of the IL-1 family, IL-37 acts as a negative regulator of inflammation. Activation of IL-37 suppresses inflammation, resulting in the suppression of inflammatory cytokines and chemokines, which in turn prevents infiltration of pro-inflammatory cells, mainly eosinophils and neutrophils. The exact molecular and cellular mechanisms of the anti-inflammatory effect of IL-37 in the development of allergic diseases (AD) have not been fully studied. This review summarizes and analyzes the accumulated experimental data on the role of IL-37 in the pathogenesis of AD, such as allergic rhinitis, bronchial asthma, and atopic dermatitis.

APA, Harvard, Vancouver, ISO, and other styles

37

Liu, Canjun, Yancui Cui, Dan Zhang, Xiao Tian, and Hongyan Zhang. "Analysis of Serum Interleukin-37 Level and Prognosis in Patients with ACS." Computational and Mathematical Methods in Medicine 2021 (September 17, 2021): 1–6. http://dx.doi.org/10.1155/2021/3755458.

Full text

Abstract:

Objective. To explore the level of serum interleukin-37 in patients with acute coronary syndrome (ACS) and its prognostic value. Methods. Altogether, 121 continuous ACS cases from September 2017 to June 2020 were selected as the research group (RG), and 107 healthy individuals during the same period were obtained as the control group (CG). ELISA was applied to test IL-37 in the serum of the CG and the RG. Chemiluminescence immunoassay was applied to test NT-pro BNP and hs-cTnI in each group and immune scattering turbidimetry to test hs-CRP. The correlation of IL-37 with serum NT-pro BNP, hs-cTnI, and CRP was analyzed, and the value of IL-37 in diagnosis and prognosis prediction of patients with ACS was tested. Logistic regression was applied to test the independent risk factors affecting poor prognosis of patients with ACS. Results. IL-37 was poorly expressed in patients with ACS, which had a high diagnostic value for ACS (sensitivity: 94.39%, specificity: 74.38%, and area under curve: 0.945). There was a negative correlation of IL-37 with serum NT-pro BNP, hs-cTnI, and CRP. IL-37 in patients with poor prognosis was markedly declined compared with that of patients with good prognosis, and the predicted AUC was 0.965. Logistic regression revealed that low IL-37, diabetes, high CRP, NT-pro BNP, and hs-cTnI in the blood were independent risk factors for poor prognosis in patients with ACS. Conclusion. IL-37 is low expressed in patients with ACS, which has a good diagnostic and prognostic value for ACS, and may be applied as an important marker for the prediction of patients with ACS.

APA, Harvard, Vancouver, ISO, and other styles

38

Ding, Liping, Li Li, Dongzhou Liu, and Zhong Huang. "The anti-inflammatory effects of interleukin-37 on active Behcet's disease." Journal of Shenzhen University Science and Engineering 33, no. 5 (2016): 447. http://dx.doi.org/10.3724/sp.j.1249.2016.05447.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Yan, Jingjing, Yuling Zhang, Shimeng Cheng, Bin Kang, Jinbiao Peng, Xiaodan Zhang, Meichun Yuan, et al. "Common genetic heterogeneity of human interleukin-37 leads to functional variance." Cellular & Molecular Immunology 14, no. 9 (September 26, 2016): 783–91. http://dx.doi.org/10.1038/cmi.2016.48.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Li, Yan, Qiaoyan Gao, Keye Xu, Xiao Peng, Xianli Yuan, Wenwen Jiang, and Mingcai Li. "Interleukin-37 Attenuates Bleomycin-Induced Pulmonary Inflammation and Fibrosis in Mice." Inflammation 41, no. 5 (June 28, 2018): 1772–79. http://dx.doi.org/10.1007/s10753-018-0820-9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Cheng, Jie, Hong Ouyang, and Jingdong Du. "Expression and Regulation of Interleukin-37 in Pathogenesis of Nasal Polyps." Indian Journal of Otolaryngology and Head & Neck Surgery 66, no. 4 (May 9, 2014): 401–6. http://dx.doi.org/10.1007/s12070-014-0725-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Shin, Hyun-Mo, Yong Rok Lee, Yoon Sook Chang, Jun-Young Lee, Byung Hak Kim, Kyung Rak Min, and Youngsoo Kim. "Suppression of interleukin-6 production in macrophages by furonaphthoquinone NFD-37." International Immunopharmacology 6, no. 6 (June 2006): 916–23. http://dx.doi.org/10.1016/j.intimp.2006.01.006.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Huang, Zhaohao, Lihui Xie, He Li, Xiuxing Liu, Joseph A. Bellanti, Song Guo Zheng, and Wenru Su. "Insight into interleukin-37: The potential therapeutic target in allergic diseases." Cytokine & Growth Factor Reviews 49 (October 2019): 32–41. http://dx.doi.org/10.1016/j.cytogfr.2019.10.003.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Navrátilová, A., V. Voclonová, H. Hulejova, L. Andres Cerezo, J. Zavada, K. Pavelka, L. Šenolt, and B. Stiburkova. "POS1142 INTERLEUKIN-37: ASSOCIATIONS OF PLASMA LEVELS AND GENETIC VARIANTS IN GOUT." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 850.2–851. http://dx.doi.org/10.1136/annrheumdis-2021-eular.3217.

Full text

Abstract:

Background:IL-37, recently characterized IL-1 family member, has anti-inflammatory effects by suppression of IL-1ß and other proinflammatory cytokines. In this study we investigated the effects of genetics variants in IL-37 link with IL-37 plasma levels in a cohorts of patients with hyperuricemia/gout.Objectives:The aim of this study was to determine the association of IL-37 gene polymorphism and plasma IL-37 levels in patients with hyperuricemia and gout.Methods:The cohorts consisted of 50 control subjects, 50 subjects of primary hyperuricemia, 50 subjects of primary gout, 28 subjects of tophaceous gout and 19 subjects of acute gout flare. The analyzed cohorts were selected from a previously reported set of 250 hyperuricemia/gout patients and 132 normouricemic subjects (1) according to the descending level of serum urate. All coding regions and intron-exon boundaries of IL-37, exon 1-5, were amplified and sequenced directly. Comparisons of presence/absence of identified variants was performed using P-values binomial test. Levels of plasma IL-37 were measured using Enzyme-Linked ImmunoSorbent Assay. All tests were performed in accordance with standards set by the institutional ethics committees, which approved the project in Prague (no.6181/2015).Results:We identified 12 IL-37 genetic variants: five intron (rs28947188, rs2466448, rs3811045, rs3811048, rs2708944), and seven non-synonymous allelic variants (rs3811046, rs3811047, rs2708943, rs2723183, rs2723187, rs2708947, rs27231927). Minor allele frequency (MAF) of those variants in European population from ExAC databases were used for comparison. Our data showed that the rs28947188, rs3811045, rs3811046, rs3811047, rs2723187, rs2708947, and rs27231927 variants were under-represented in the Czech hyperuricemia, gout, and tophaceous gout cohort compared with the control cohort and general European population (P = 0.0082 – 0.0395).The levels of plasma IL-37 were significantly higher in patients with tophaceous gout compared to control subjects (P 0.0329) whereas no changes were observed in subjects with primary hyperuricemia, primary gout or acute gout flare compared to control subjects. However, IL-37 was elevated in cohorts of patients with gout, tophaceous gout and acute gout flare compared to primary hyperuricemia subjects (P 0.0198, 0.0005, 0.0099; respectively).Conclusion:Although further analyzes are needed to elucidate the role of IL-37 in the gout, our results show that genetic variants in anti-inflammatory cytokine IL-37 are probably implicated in the pathogenesis of gout.References:[1]Toyoda Y, et al. Functional characterization of clinically-relevant rare variants in ABCG2 identified in a gout and hyperuricemia cohort. Cells. 2019 Apr 18;8(4).Acknowledgements:This study was supported by the grant from the Czech Republic Ministry of Health RVO 00023728.Disclosure of Interests:None declared.

APA, Harvard, Vancouver, ISO, and other styles

45

Zhu, Ruirui, Fangyuan Zhang, Chengliang Pan, Kunwu Yu, Yucheng Zhong, and Qiutang Zeng. "Role of IL-37- and IL-37-Treated Dendritic Cells in Acute Coronary Syndrome." Oxidative Medicine and Cellular Longevity 2021 (August 21, 2021): 1–9. http://dx.doi.org/10.1155/2021/6454177.

Full text

Abstract:

As a chronic inflammatory disease, atherosclerosis is a leading cause of morbidity and mortality in most countries. Inflammation is responsible for plaque instability and the subsequent onset of acute coronary syndrome (ACS), which is one of the leading causes of hospitalization. Therefore, exploring the potential mechanism underlying ACS is of considerable concern, and searching for alternative therapeutic targets is very urgent. Interleukin-37 (IL-37) inhibits the production of proinflammatory chemokines and cytokines and acts as a natural inhibitor of innate and adaptive immunity. Interestingly, our previous study with murine models showed that IL-37 alleviated cardiac remodeling and myocardial ischemia/reperfusion injury. Of note, our clinical study revealed that IL-37 is elevated and plays a beneficial role in patients with ACS. Moreover, dendritic cells (DCs) orchestrate both immunity and tolerance, and tolerogenic DCs (tDCs) are characterized by more secretion of immunosuppressive cytokines. As expected, IL-37-treated DCs are tolerogenic. Hence, we speculate that IL-37- or IL-37-treated DCs is a novel therapeutic possibility for ACS, and the precise mechanism of IL-37 requires further study.

APA, Harvard, Vancouver, ISO, and other styles

46

Wang, Lulu, Zheng Liu, Dongni Huang, Yuxin Ran, Hanwen Zhang, Jie He, Nanlin Yin, and Hongbo Qi. "IL-37 Exerts Anti-Inflammatory Effects in Fetal Membranes of Spontaneous Preterm Birth via the NF-κB and IL-6/STAT3 Signaling Pathway." Mediators of Inflammation 2020 (July 11, 2020): 1–15. http://dx.doi.org/10.1155/2020/1069563.

Full text

Abstract:

Spontaneous preterm birth (sPTB), defined as delivery before 37 weeks of gestation, is thought to be a multifactorial syndrome. However, the inflammatory imbalance at the maternal-fetal interface promotes excessive secretion of inflammatory factors and induces apoptosis and degradation of the extracellular matrix (ECM), which can subsequently lead to preterm birth. As an anti-inflammatory molecule in the IL-1 family, interleukin-37 (IL-37) mainly plays an inhibiting role in a variety of inflammatory diseases. However, as a typical inflammatory disease, no previous studies have been carried out to explore the role of IL-37 in sPTB. In this study, a series of molecular biological experiments were performed in clinical samples and human amniotic epithelial cell line (Wistar Institute Susan Hayflick (WISH)) to investigate the deficiency role of IL-37 and the potential mechanism. Firstly, the results indicated that the expression of IL-37 in human peripheral plasma and fetal membranes was significantly decreased in the sPTB group. Afterward, it is proved that IL-37 could significantly suppress the production of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in WISH cells. Simultaneously, once silence IL-37, LPS-induced apoptosis and activity of matrix metalloproteinases (MMPs) 2 and 9 were significantly increased. In addition, the western blot data showed that IL-37 performed its biological effects by inhibiting the NF-κB and IL-6/STAT3 pathway. In conclusion, our results suggest that IL-37 limits excessive inflammation and subsequently inhibits ECM remodeling and apoptosis through the NF-κB and IL-6/STAT3 signaling pathway in the fetal membranes.

APA, Harvard, Vancouver, ISO, and other styles

47

Liu, Haipeng, and Baoxue Ge. "Interleukin-37: a new molecular target for host-directed therapy of tuberculosis." Future Microbiology 12, no. 6 (May 2017): 465–68. http://dx.doi.org/10.2217/fmb-2017-0030.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

Meng, Jiang-Ping, Peng Luo, Yao Bai, and Fang Cui. "Entecavir downregulates interleukin-37 in patients with chronic active hepatitis B infection." Journal of International Medical Research 48, no. 1 (January 2020): 030006051988415. http://dx.doi.org/10.1177/0300060519884157.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

Jia, Yuning, Shoaib Anwaar, Linyun Li, Zhihua Yin, Zhizhon Ye, and Zhong Huang. "A new target for the treatment of inflammatory bowel disease: Interleukin-37." International Immunopharmacology 83 (June 2020): 106391. http://dx.doi.org/10.1016/j.intimp.2020.106391.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Weidlich, Simon, Ana-Maria Bulau, Tobias Schwerd, Johanna Helmbrecht, Martin Lacher, Doris Mayr, Sibylle Koletzko, and Philip Bufler. "CS10-6. Expression of Interleukin-37 in human pediatric inflammatory bowel disease." Cytokine 56, no. 1 (October 2011): 59. http://dx.doi.org/10.1016/j.cyto.2011.07.366.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Journal articles on the topic 'Interleukin 37'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles