Relevant bibliographies by topics / IL-17B

Academic literature on the topic 'IL-17B'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "IL-17B"

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Li, Yunyan, Jianfu Chen, Yuan Yang, Yuxue Wang, Yong Zhang, Yan Zhou, Yan Bao, Zongmei Zhang, and Yongping Lu. "Necroptosis Plays a Crucial Role in Vascular Injury during DVT and Is Enhanced by IL-17B." Journal of Immunology Research 2022 (August 19, 2022): 1–15. http://dx.doi.org/10.1155/2022/6909764.

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Background. This study investigated whether vascular endothelial necroptosis is involved in deep vein thrombosis (DVT) and how IL-17B facilitates necroptosis signaling. Methods. The DVT mouse model was induced by ligation of the IVC. The cross-sectional area of thrombus increases and the thrombus occupied the entire venous lumen at 48 h after ligation. Meanwhile, the increased expression of p-RIP3/RIP3 was most pronounced at 48 h after ligation, and the p-MLKL/MLKL peaked at 72 h. Results. Based on Illumina sequencing and KEGG pathway analyses, the activated RIP3/MLKL is associated with increased IL-17B. With thrombus formation, IL-17B was upregulated and enhanced the expression of RIP3 and MLKL in the IVC wall, as well as their phosphorylation levels (all P < 0.05 , the comparison group consisted of the control group, DVT group, DVT/IL-17B group, and DVT/anti-IL-17B group). The p-RIP3/RIP3 and p-MLKL/MLKL ratios were reduced by anti-IL-17B. Similarly, the weight and cross-sectional area of the thrombi were increased by IL-17B and decreased by the IL-17B antibody. IL-17B had a smaller effect on thrombosis in knockout mice compared with WT mice. In vitro, the IL-17B protein expression and the level of RIP3 and MLKL phosphorylation increased high in the OGD cells, accompanied by increased expression of IL-6 and TNF-α. IL-17B enhanced the expression of IL-6 and TNF-α but had little effect on the IL-6 and TNF-α after transfected with siRIP3 or siMLKL. Similarly, the plasma IL-17B, IL-6, and TNF-α were significantly increased after thrombosis in WT mice, and enhanced by IL-17B. But IL-17B did not increase the plasma IL-6 and TNF-α in knockout mice. Conclusions. In conclusion, those results suggest that vascular endothelial necroptosis plays a crucial role in vascular injury and IL-17B could enhance the necroptosis pathway.
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Bie, Qingli, Hui Song, Xinke Chen, Xiao Yang, Shuo Shi, Lihua Zhang, Rou Zhao, et al. "IL-17B/IL-17RB signaling cascade contributes to self-renewal and tumorigenesis of cancer stem cells by regulating Beclin-1 ubiquitination." Oncogene 40, no. 12 (March 1, 2021): 2200–2216. http://dx.doi.org/10.1038/s41388-021-01699-4.

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AbstractCancer stem cells (CSCs) are characterized by robust self-renewal and tumorigenesis and are responsible for metastasis, drug resistance, and angiogenesis. However, the molecular mechanisms for the regulation of CSC homeostasis are incompletely understood. This study demonstrated that the interleukin-17 (IL-17)B/IL-17RB signaling cascade promotes the self-renewal and tumorigenesis of CSCs by inducing Beclin-1 ubiquitination. We found that IL-17RB expression was significantly upregulated in spheroid cells and Lgr5-positive cells from the same tumor tissues of patients with gastric cancer (GC), which was closely correlated with the degree of cancer cell differentiation. Recombinant IL-17B (rIL-17B) promoted the sphere-formation ability of CSCs in vitro and enhanced tumor growth and metastasis in vivo. Interestingly, IL-17B induced autophagosome formation and cleavage-mediated transformation of LC3 in CSCs and 293T cells. Furthermore, inhibition of autophagy activation by ATG7 knockdown reversed rIL-17B-induced self-renewal of GC cells. In addition, we showed that IL-17B also promoted K63-mediated ubiquitination of Beclin-1 by mediating the binding of tumor necrosis factor receptor-associated factor 6 to Beclin-1. Silencing IL-17RB expression abrogated the effects of IL-17B on Beclin-1 ubiquitination and autophagy activation in GC cells. Finally, we showed that IL-17B level in the serum of GC patients was positively correlated with IL-17RB expression in GC tissues, and IL-17B could induce IL-17RB expression in GC cells. Overall, the results elucidate the novel functions of IL-17B for CSCs and suggest that the intervention of the IL-17B/IL-17RB signaling pathway may provide new therapeutic targets for the treatment of cancer.
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Li, Yunyan, Yuan Yang, Jianfu Chen, Yuxue Wang, Yong Zhang, Yan Zhou, Zilong Wang, and Yongping Lu. "IL-17B Regulates Endothelial Cell Apoptosis in Venous Thrombosis." Nanoscience and Nanotechnology Letters 12, no. 9 (September 1, 2020): 1106–13. http://dx.doi.org/10.1166/nnl.2020.3212.

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Venous thromboembolism (VTE) is the comorbidity of deep vein thrombosis (DVT) and pulmonary embolism (PE); it is an urgent public health problem. The primary cause of venous thrombosis is endothelial dysfunction caused by vascular injury and inflammation or overexpressed procoagulant factors. Previous studies have shown that vascular endothelial cell apoptosis is involved in venous thrombosis, causing vascular wall damage. The pro-inflammatory cytokine interleukin-17 (Il-17A) induces endothelial cell apoptosis and promotes thrombosis. However, it remains unclear whether other IL-17 family cytokines are involved in thrombus formation. Among the IL-17 family, IL-17B is less well-characterized. Several studies have reported that IL-17B could stimulate TNF-α, IL-1, and IL-6 expression in macrophages. Furthermore, IL-17B induced activation of the ERK1/2 pathway, upregulating Bcl-2 family anti-apoptotic proteins in breast tumors. However, it is unclear whether IL-17B is involved in thrombus formation by regulating endothelial apoptosis. Therefore, this study aimed to examine whether IL-17B could affect endothelial apoptosis by promoting thrombus formation.
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Sanders, Andrew J., Xiaoxia Guo, Malcolm D. Mason, and Wen G. Jiang. "IL-17B Can Impact on Endothelial Cellular Traits Linked to Tumour Angiogenesis." Journal of Oncology 2010 (2010): 1–5. http://dx.doi.org/10.1155/2010/817375.

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IL-17B is a member of the IL-17 cytokine family which have been implicated in inflammatory response and autoimmune diseases such as rheumatoid arthritis. The founding member of this family, IL-17 (or IL-17A), has also been implicated in promoting tumour angiogenesis through the induction of other proangiogenic factors. Here we examine the potential of recombinant human IL-17B to contribute to the angiogenic process. In vitro rhIL-17B was able to inhibit HECV endothelial cell-matrix adhesion and cellular migration and also, at higher concentrations, could substantially reduce tubule formation compared to untreated HECV cells in a Matrigel tubule formation assay. This data suggests that IL-17B may act in an antiangiogenic manner.
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Li, Jiahui, Xiaolin Wu, Lars Schiffmann, Thomas MacVicar, Chenghui Zhou, Zhefang Wang, Dai Li, et al. "IL-17B/RB Activation in Pancreatic Stellate Cells Promotes Pancreatic Cancer Metabolism and Growth." Cancers 13, no. 21 (October 24, 2021): 5338. http://dx.doi.org/10.3390/cancers13215338.

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In pancreatic ductal adenocarcinoma (PDAC), the tumor stroma constitutes most of the cell mass and contributes to therapy resistance and progression. Here we show a hitherto unknown metabolic cooperation between pancreatic stellate cells (PSCs) and tumor cells through Interleukin 17B/Interleukin 17B receptor (IL-17B/IL-17RB) signaling. Tumor-derived IL-17B carrying extracellular vesicles (EVs) activated stromal PSCs and induced the expression of IL-17RB. PSCs increased oxidative phosphorylation while reducing mitochondrial turnover. PSCs activated tumor cells in a feedback loop. Tumor cells subsequently increased oxidative phosphorylation and decreased glycolysis partially via IL-6. In vivo, IL-17RB overexpression in PSCs accelerated tumor growth in a co-injection xenograft mouse model. Our results demonstrate a tumor-to-stroma feedback loop increasing tumor metabolism to accelerate tumor growth under optimal nutritional conditions.
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Wu, Heng-Hsiung, Wendy W. Hwang-Verslues, Wen-Hsin Lee, Chun-Kai Huang, Pei-Chi Wei, Chia-Lin Chen, Jin-Yuh Shew, et al. "Targeting IL-17B–IL-17RB signaling with an anti–IL-17RB antibody blocks pancreatic cancer metastasis by silencing multiple chemokines." Journal of Experimental Medicine 212, no. 3 (March 2, 2015): 333–49. http://dx.doi.org/10.1084/jem.20141702.

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Pancreatic cancer has an extremely high mortality rate due to its aggressive metastatic nature. Resolving the underlying mechanisms will be crucial for treatment. Here, we found that overexpression of IL-17B receptor (IL-17RB) strongly correlated with postoperative metastasis and inversely correlated with progression-free survival in pancreatic cancer patients. Consistently, results from ex vivo experiments further validated that IL-17RB and its ligand, IL-17B, plays an essential role in pancreatic cancer metastasis and malignancy. Signals from IL-17B–IL-17RB activated CCL20/CXCL1/IL-8/TFF1 chemokine expressions via the ERK1/2 pathway to promote cancer cell invasion, macrophage and endothelial cell recruitment at primary sites, and cancer cell survival at distant organs. Treatment with a newly derived monoclonal antibody against IL-17RB blocked tumor metastasis and promoted survival in a mouse xenograft model. These findings not only illustrate a key mechanism underlying the highly aggressive characteristics of pancreatic cancer but also provide a practical approach to tackle this disease.
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Guo, Shaohua, Junjie Peng, Yongle Xiao, Yanyan Liu, Weiwei Hao, Xin Yang, Hongning Wang, and Rong Gao. "The Construction and Immunoadjuvant Activities of the Oral Interleukin-17B Expressed by Lactobacillus plantarum NC8 Strain in the Infectious Bronchitis Virus Vaccination of Chickens." Vaccines 8, no. 2 (June 6, 2020): 282. http://dx.doi.org/10.3390/vaccines8020282.

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Interleukin-17B (IL-17B) is a protective cytokine of the IL-17 family and plays an essential role in the regulation of mucosal inflammation. However, little is known about the role of IL-17B in the control of viral infections. In this study, a recombinant Lactobacillus plantarum, designated as NC8-ChIL17B, was constructed to express the chicken IL-17B (ChIL-17B) gene. The recombinant ChIL17B (rChIL17B) protein was about 14 kDa and was anchored to the surface of NC8 cells. In vitro, it was found that the rChIL17B protein inhibited the proliferation of the infectious bronchitis virus (IBV) through activation of nuclear factor kappa B (NF-κB) and the JAK (Janus kinase)-STAT (signal transducers and activators of transcription) signaling. Moreover, to evaluate the immunoadjuvant activities of NC8-ChIL17B, 40 three-day-old specific pathogen-free (SPF) chickens were divided into four groups. Three groups were orally vaccinated with fresh NC8, NC8-ChIL17B, and phosphate buffered saline (PBS), along with the infectious bronchitis virus vaccine, and the other group was the PBS-negative control. The results of the IBV-specific antibody titer and the concentration of the cytokines IL-2, IL-4, IL-6, and interferon gamma (IFN-γ) in sera, as well as the concentration of secretory immunoglobulin A (sIgA) in the tracheal and small intestinal mucosa, the number of cluster of differentiation 4 positive (CD4+) and cluster of differentiation 8 positive (CD8+) T cells in the blood, and the expression of immune-related genes all indicated that NC8-ChIL17B efficiently enhanced the humoral and cellular immune responses to IBV vaccine. Moreover, the viral loads in the NC8-ChIL17B- and IBV-vaccinated group were significantly lower than in the control groups, suggesting a significant promotion of the immunoprotection of IBV vaccination against the virulent IBV strain. Therefore, ChIL-17B is a promising, effective adjuvant candidate for chicken virus vaccines.
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Bie, Qingli, Chengqiang Jin, Bin Zhang, and Haixin Dong. "IL-17B: A new area of study in the IL-17 family." Molecular Immunology 90 (October 2017): 50–56. http://dx.doi.org/10.1016/j.molimm.2017.07.004.

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Zhang, Shuxia, Li Wu, Jiawei Chen, Jiatian Wei, Haiming Cai, Miaopeng Ma, Peijing Zhao, et al. "Effects of porcine IL-17B and IL-17E against intestinal pathogenic microorganism." Molecular Immunology 116 (December 2019): 151–59. http://dx.doi.org/10.1016/j.molimm.2019.10.011.

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Singh, Ram Pyare, Bevra Hahn, and Awlad Hossain. "Expression of Interferon-inducible Genes is Influenced by Sex Hormones in SLE." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 210.12. http://dx.doi.org/10.4049/jimmunol.196.supp.210.12.

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Abstract SLE is a female-biased disease with female to male ratio of 9:1. Accumulating evidence suggests the existence of a nexus between inflammatory pathways and 17b-estradiol, resulting in increased interferon stimulated genes (ISGs), autoantibodies and dysregulation of immune cells in SLE. However, the mechanisms by which 17b-estradiol interacts with IFN and T cells, B cells and antigen presenting cells (APC) in SLE is poorly understood. Women may be more susceptible than men to SLE and other autoimmune diseases in part because many healthy women have higher interferon regulated genes. Similarly, female BWF1 lupus mice have increased expression of interferon genes compared to age and sex- matched males. We found that plasma estradiol levels positively correlated with levels of serum/plasma IL-6, and 21/IL-23 in SLE patients. Plasma 17b-estradiol levels are significantly increased in female SLE patients compared to healthy females (p&lt;0.01). Furthermore, we found that estradiol increases proinflammatory cytokines, and level of estradiol positively correlated with expression of miR21, 25, and 186 in SLE patients. Expression of miR21, miR25 and miR186 are positively correlated with SLEDAI score in SLE. Understanding the role of 17b-estradiol in the regulation of pro-inflammatory pathways, ISGs, and microRNAs will further advance our understanding of SLE disease pathology and may identify additional novel therapeutic targets.
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Dissertations / Theses on the topic "IL-17B"

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Silva, Fabio Arruda e. "Molecular Mechanisms Regulating Cytokine Production by Human Neutrophils." Doctoral thesis, 2018. http://hdl.handle.net/11562/984950.

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Neutrophils are known to perform a series of effector functions that are crucial for the innate and adaptive responses towards infections. Furthermore, neutrophils respond to various stimuli, including microbial components, by synthetizing and secreting a variety of cytokines. In this context, the main objective of this study was to re-evaluate the capacity of human neutrophils to express and produce cytokines of the IL-17 family, including IL-17A, IL-17B, IL-17F and IL-17AF since the current literature on this topic is discordant. By performing RT-qPCR, immunohistochemistry (IHC), immunoblotting, protein measurement via commercial ELISA, chromatin immunoprecipitation (ChIP) and ChIP-seq, we evaluated transcriptional and epigenetic regulation, as well as production of the latter cytokines by highly pure (> 99.7 %) populations of human neutrophils. In agreement with some published data, we found that neutrophils do not express/produce IL-17A, IL-17F, IL-17AF or IL-17B mRNA/protein upon incubation with a variety of agonists. Similar findings were observed by analyzing neutrophils obtained from active psoriatic patients. No IL-17A and IL-17F mRNA expression/production was found even when human neutrophils from healthy donors were incubated with IL-6 plus IL-23 at very elevated concentrations in combination with inactivated hyphae or conidia from Aspergillus fumigatus, unlike shown in multiple studies. Moreover, consistent with the inability of human neutrophils to express IL-17A and IL-17F mRNA, no deposition of H3K27Ac and H3K4me1, which are histone marks of, respectively, active and poised genomic regulatory elements, was detected at the IL-17A/F genomic locus in resting or IL-6 plus IL-23-stimulated neutrophils. In addition, although we found that anti-IL-17A and anti-IL-17B commercial antibodies positively stained cytospin preparations of resting and activated neutrophils by IHC, these antibodies do not recognize any intracellular protein having the correct MW of either IL-17A or IL-17B in corresponding lysates of the same neutrophil preparations by immunoblotting. Since the same antibodies were found to strongly stain other intracellular proteins of neutrophils, we conclude that their ability to positively stain neutrophils derives from IL-17A- or IL-17B-independent unspecific binding. In conclusion, our data not only confirm and further support our previous original findings on the inability of human neutrophils to express/produce IL-17A, IL-17B and IL-17F mRNAs/proteins, but also attempt to explain why other published studies continue to report the opposite.
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Book chapters on the topic "IL-17B"

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Evans Adunyah, Samuel, Richard Akomeah, Fareed K.N. Arthur, Roland S. Cooper, and Joshua C.M. Williams. "IL-17 Biological Effects and Signaling Mechanisms in Human Leukemia U937 Cells." In Interleukins - The Immune and Non-Immune Systems’ Related Cytokines. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96422.

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Human Interlekin-17 is produced by memory activated CD4+ T cells and other cells. It was initially considered unique in that its specific receptor is distinct from other cytokine receptors. IL-17 receptor is ubiquitously expressed by different cells including T cells. IL-17 plays a role in regulating growth, immune response and pro-inflammatory responses. It regulates differentiation of a subset of Th0 cells into Th-17 cells, which produce IL-17-induced cytokines. The IL-17R belongs to type 1 cytokine receptors. IL-17 belongs to a superfamily of its own, which includes IL-17A, IL-17B, IL-17C, IL-17E and IL-17F. These members of IL-17 superfamily have some sequence homology but bind to different receptors. Prior to this investigation, limited information existed on the effects of IL-17A in human leukemia cell lines. Our results show that IL-17A promotes growth, anti-apoptotic effects, chemotaxis, cytokine expression and transcriptional factor activation in leukemia cells. IL-17A activates multiple signaling pathways including PI-3 K, Jak–STAT, Raf-ERK1/2 and SRC kinase pathways, which mediate different biological effects of IL-17A in leukemia cells. Our findings implicate IL-17A in leukemia cell growth and survival, supporting potential leukemia therapy via development of anti-IL-17A drugs. This chapter focuses on IL-17A, herein referred to as IL-17.
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Conference papers on the topic "IL-17B"

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Laprevotte, Emilie, Aurélie Docquier, Jeremy Bastid, Cécile Déjou, Marion Lapierre, Gilles Alberici, Armand Bensussan, Jean-François Eliaou, and Nathalie Bonnefoy. "Abstract 1602: Generation of anti-IL-17B antibodies neutralizing IL-17B-mediated alterations of the immune microenvironment, promotion of tumor cell initiating capacity and chemoresistance." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1602.

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Liang, Chi-Ming, Ching-Chun Liao, and Shu-Mei Liang. "Abstract 3855: Refolded albumin inhibits IL-17B-driven pancreatic cancer migration." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3855.

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Sanders, AJ, RE Mansel, MD Mason, and WG Jiang. "P4-09-20: Expression Profile of Interleukin 17B and the Receptor IL-17BR in Clinical Breast Cancer." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p4-09-20.

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