Статті в журналах: "IL-17B"

1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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<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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11

Singh, Ram Pyare, and Bevra H. Hahn. "Expression of Interferon Genes is Influenced by Sex Hormones in SLE." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 132.10. http://dx.doi.org/10.4049/jimmunol.202.supp.132.10.

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Abstract Environmental factors, genetic defects, miRNA dysregulation, and hormonal factors can influence susceptibility to SLE. Estradiol has been shown to increase the expression of interferon genes and pathways and thus could promote susceptibility to the disease in women. Recent 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. The mechanisms by which 17b-estradiol interacts with IFN and various immune cells in SLE is poorly understood. The goal of this study is to determine the role of estradiol in the regulation of candidate target genes, miRNAs, and mechanisms of regulation of autoantibody production in SLE. Women may be more susceptible than men to SLE and other autoimmune diseases in part because many healthy women have higher interferon-regulated genes. 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<0.01). Furthermore, we found that estradiol increases pro-inflammatory cytokines, and level of estradiol positively correlated with expression of miR21, 25, and 186 in SLE patients. Expression of miR21, 25, and 186 are positively correlated with SLEDAI score in SLE. We also found that expression of interferon genes (IL-12, 17, 21) is influenced by sex hormones 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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12

Robak, Ewa, Zofia Gerlicz-Kowalczuk, Bożena Dziankowska-Bartkowiak, Anna Wozniacka, and Jaroslaw Bogaczewicz. "Serum concentrations of IL-17A, IL-17B, IL-17E and IL-17F in patients with systemic sclerosis." Archives of Medical Science 15, no. 3 (2019): 706–12. http://dx.doi.org/10.5114/aoms.2019.84738.

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13

Singh, Ram Pyare, and Bevra H. Hahn. "Interferon Genes are Influenced by Sex Hormones (17b-estradiol) in SLE." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 236.19. http://dx.doi.org/10.4049/jimmunol.204.supp.236.19.

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Abstract Environmental factors, genetic defects, miRNA dysregulation, and hormonal factors can influence susceptibility to SLE. Estradiol has been shown to increase the expression of interferon genes and pathways and thus could promote susceptibility to the disease in women. Recent 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. The mechanisms by which 17b-estradiol interacts with IFN and various immune cells in SLE is poorly understood. Aim is to determine the role of estradiol in the regulation of candidate target genes and miRNAs and mechanisms of regulation of autoantibody production in SLE. Women may be more susceptible than men to SLE and other autoimmune diseases in part because many healthy women have higher interferon regulated genes. 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<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. We found that expression of interferon genes is influenced by sex hormones 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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14

Lajoie-Kadoch, Stéphane, Philippe Joubert, Séverine Létuvé, Andrew J. Halayko, James G. Martin, Abdellilah Soussi-Gounni та Qutayba Hamid. "TNF-α and IFN-γ inversely modulate expression of the IL-17E receptor in airway smooth muscle cells". American Journal of Physiology-Lung Cellular and Molecular Physiology 290, № 6 (червень 2006): L1238—L1246. http://dx.doi.org/10.1152/ajplung.00301.2005.

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The interleukin-17B receptor (IL-17BR) is expressed in a variety of tissues and is upregulated under inflammatory conditions. This receptor binds both its cognate ligand IL-17B and IL-17E/IL-25, a novel cytokine known to promote Th2 responses. The present study shows that airway smooth muscle cells express IL-17BR in vitro and that its expression is upregulated by TNF-α and downregulated by IFN-γ. Our data indicate that TNF-α upregulates IL-17BR mainly through nuclear factor-κB as assessed with the IκB kinase 2 inhibitor AS-602868. In addition, both IFN-γ and dexamethasone are able to antagonize a TNF-α-induced IL-17BR increase in mRNA expression. The mitogen-activated protein kinase kinase inhibitor U0126 totally reversed the inhibition observed with IFN-γ, suggesting the involvement of the extracellular signal-regulated kinase pathway in this effect. In addition, on stimulation with IL-17E, airway smooth muscle cells increase their expression of ECM components, namely procollagen-αI and lumican mRNA. Furthermore, immunohistochemical analysis of biopsies from asthmatic subjects reveals that this receptor is abundant in smooth muscle layers. This is the first report showing IL-17BR receptor in structural cells of the airways. Our results suggest a potential proremodeling effect of IL-17E on airway smooth muscle cells through the induction of ECM and that its receptor is upregulated by proinflammatory conditions.

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15

Kokubu, Takeshi, Dominik R. Haudenschild, Timothy A. Moseley, Larry Rose, and A. Hari Reddi. "Immunolocalization of IL-17A, IL-17B, and Their Receptors in Chondrocytes During Fracture Healing." Journal of Histochemistry & Cytochemistry 56, no. 2 (October 15, 2007): 89–95. http://dx.doi.org/10.1369/jhc.7a7223.2007.

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16

Sanders, A., S. Cai, S. Owen, K. Ji, Y. Jia, S. Jia, J. Ji, and W. Jiang. "Potential implication of IL-17B and IL-17RB in the progression of gastric cancer." European Journal of Cancer 72 (February 2017): S87. http://dx.doi.org/10.1016/s0959-8049(17)30367-2.

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17

Duruöz, M. T., Ü. Uçar, Y. Guvenç, and Z. Sari Sürmeli. "AB0117 Evaluation of serum levels of interleukin(il)-17a, il-17b, il-17c, il-17f and il-23 levels in psoriatic arthritis." Annals of the Rheumatic Diseases 72, Suppl 3 (June 2013): A821.2—A821. http://dx.doi.org/10.1136/annrheumdis-2013-eular.2440.

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18

Ramirez-Carrozzi, Vladimir, Naruhisa Ota, Arivazhagan Sambandam, Kit Wong, Jason Hackney, Nadia Martinez-Martin, Wenjun Ouyang, and Rajita Pappu. "Cutting Edge: IL-17B Uses IL-17RA and IL-17RB to Induce Type 2 Inflammation from Human Lymphocytes." Journal of Immunology 202, no. 7 (February 15, 2019): 1935–41. http://dx.doi.org/10.4049/jimmunol.1800696.

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19

Li, H., J. Chen, A. Huang, J. Stinson, S. Heldens, J. Foster, P. Dowd, A. L. Gurney, and W. I. Wood. "Cloning and characterization of IL-17B and IL-17C, two new members of the IL-17 cytokine family." Proceedings of the National Academy of Sciences 97, no. 2 (January 18, 2000): 773–78. http://dx.doi.org/10.1073/pnas.97.2.773.

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20

Liu, Yuwan, Zewei Shao, Guoqiang Shangguan, Qingli Bie, and Bin Zhang. "Biological Properties and the Role of IL-25 in Disease Pathogenesis." Journal of Immunology Research 2018 (September 23, 2018): 1–8. http://dx.doi.org/10.1155/2018/6519465.

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The interleukin- (IL-) 17 superfamily, a T cell-derived cytokine, consists of 6 ligands (IL-17A–IL-17F) and 5 receptors (IL-17RA–IL-17RE). IL-17A, a prototype member of this family, is involved in the pathogenesis of allergies, autoimmune diseases, allograft transplantations, and malignancies. By contrast, IL-17B is reported to be closely related to certain diseases, particularly tumors such as breast cancer, gastric cancer, and pancreatic cancer. Recently, the biological function of IL-17E (also called IL-25) in disease, particularly airway diseases, has attracted the attention of researchers. However, studies on IL-25 are scant. In this review, we detail the structural characteristics, expression patterns, responder cells, biological properties, and role of IL-25 in disease pathogenesis.

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Lechner, Christian J., Beate Grüner, Xiangsheng Huang, Wolfgang H. Hoffmann, Peter Kern, and Peter T. Soboslay. "Parasite-Specific IL-17-Type Cytokine Responses and Soluble IL-17 Receptor Levels in Alveolar Echinococcosis Patients." Clinical and Developmental Immunology 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/735342.

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Alveolar Echinococcosis (AE) caused by the cestodeEchinococcus multilocularis, is a severe helminth infection of man, where unrestricted parasite growth will ultimately result in organ failure and fatality. The tissue-infiltrative growth of the larval metacestode and the limited efficacy of available drugs complicate successful intervention in AE; patients often need life-long medication, and if possible, surgical resection of affected tissues and organs. Resistance to AE has been reported, but the determinants which confer protection are not known. ln this study, we analyzed in patients at distinct stages of Alveolar Echirococcosis, that is cured, stable and progressive AE, as well as in infection-free controls, the cellular production and plasma levels of pro-inflammatory cytokines lL-17A, lL-17B, lL-17F and their soluble receptors lL-17RA (slL-17RA) and IL-17RB (sIL-17RB). Significantly elevated levels of IL-17B and slL-17RB were observed, whilst lL-17F and slL-17RA were reduced in patients with AE. Similarly, the cellular production of lL-17F and slL-L7RA in response toE. multilocularisantigens was low in AE patients, while levels of slL-17RB were highly enhanced. These observations suggest immune-modulating properties ofE. multitocularison lL-17 cytokine-mediated pro-inflammatory immune responses; this may facilitate the tissue infiltrative growth of the parasite and its persistence in the human host.

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Zhou, Jie, Lei Ren, Dapeng Chen, Xue Lin, Shifeng Huang, Yibing Yin, and Ju Cao. "IL-17B is elevated in patients with pneumonia and mediates IL-8 production in bronchial epithelial cells." Clinical Immunology 175 (February 2017): 91–98. http://dx.doi.org/10.1016/j.clim.2016.12.008.

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Yang, Yi-Fang, Yi-Chen Lee, Steven Lo, Yi-Ning Chung, Ya-Ching Hsieh, Wen-Chin Chiu та Shyng-Shiou F. Yuan. "A positive feedback loop of IL-17B-IL-17RB activates ERK/β-catenin to promote lung cancer metastasis". Cancer Letters 422 (травень 2018): 44–55. http://dx.doi.org/10.1016/j.canlet.2018.02.037.

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Wu, Dawei, Sarina K. Mueller, Angela L. Nocera, Kristen Finn, Towia A. Libermann, and Benjamin S. Bleier. "TREM-1 Neutrophil Activation Pathway Is Suppressed in Eosinophilic Nasal Polyps." American Journal of Rhinology & Allergy 32, no. 5 (July 2, 2018): 359–68. http://dx.doi.org/10.1177/1945892418782233.

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Background Chronic rhinosinusitis with nasal polyps (CRSwNP) is characterized by type 2 helper T-cell-skewed immune profiles, but the state of the neutrophil activation signaling pathway in CRSwNP is unknown. The purpose of this study was to examine neutrophil activation pathways in the pathogenesis of CRSwNP. Methods Institutional review board approved the study in which tissue proteomes were compared between control (inferior turbinate) and CRSwNP (nasal polyps) (n = 10/group) using an aptamer-based proteomic array and confirmed by whole transcriptomic analysis. Protein expression was analyzed using Student’s t test and Benjamini–Hochberg procedures followed by the application of Ingenuity Pathway, MetaCore, and Genemania bioinformatics analyses. Results All the patients with CRSwNP (n = 10) had eosinophilic nasal polyps. Compared with controls, proteins associated with the triggering receptor expressed on myeloid cells 1 (TREM-1) neutrophil activation signaling pathway such as Calcineurin B, zeta chain-associated protein kinase of 70 kD (ZAP70), 14-3-3 protein theta, 14-3-3 protein zeta/delta, protein kinase C delta type (PKC-D), Interleukin (IL)-17B, IL-17B receptor, IL-23, and IL-1B were significantly decreased in CRSwNP (fold change [FC] = −1.60, P = .003; FC = −1.85, P = .040; FC = −1.26, P < .001; FC = −1.05, P = .008; and FC = −1.31, P = .004; FC = −1.22, P < .001; FC = −1.09, P = .022; FC = −1.25, P < .001; and FC = −1.31, P = .014; respectively). In contrast, tissue eosinophil count ( P < .001) and eosinophil-associated proteins such as C-C motif chemokine 17, periostin, and galectin 10 were all significantly increased in CRSwNP (FC = 1.56, P = .009; FC = 3.95, P < .001; and FC = 2.44, P < .001; respectively). Furthermore, the FC of the studied proteins’ expression significantly and positively correlated with FC of their mRNA expression ( P = .001, r = .75). Conclusions TREM-1-associated neutrophilic signaling pathway proteins are significantly suppressed in eosinophilic CRSwNP.

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Bie, Qingli, Bin Zhang, Caixia Sun, Xiaoyun Ji, Prince Amoah Barnie, Chen Qi, Jingjing Peng, et al. "IL-17B activated mesenchymal stem cells enhance proliferation and migration of gastric cancer cells." Oncotarget 8, no. 12 (January 27, 2017): 18914–23. http://dx.doi.org/10.18632/oncotarget.14835.

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Yamaguchi, Yumi, Keishi Fujio, Hirofumi Shoda, Akiko Okamoto, Nelson H. Tsuno, Koki Takahashi та Kazuhiko Yamamoto. "IL-17B and IL-17C Are Associated with TNF-α Production and Contribute to the Exacerbation of Inflammatory Arthritis". Journal of Immunology 179, № 10 (2 листопада 2007): 7128–36. http://dx.doi.org/10.4049/jimmunol.179.10.7128.

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Robak, Ewa, Lilianna Kulczycka-Siennicka, Zofia Gerlicz, Monika Kierstan, Anna Korycka-Wolowiec, and Anna Sysa-Jedrzejowska. "Correlations between concentrations of interleukin (IL)-17A, IL-17B and IL-17F, and endothelial cells and proangiogenic cytokines in systemic lupus erythematosus patients." European Cytokine Network 24, no. 1 (March 2013): 60–68. http://dx.doi.org/10.1684/ecn.2013.0330.

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Yong, Tracer, Ko-Keng Chang, Yi-Sheng Wang, and Che Ma. "Active Humoral Response Reverts Tumorigenicity through Disruption of Key Signaling Pathway." Vaccines 10, no. 2 (January 21, 2022): 163. http://dx.doi.org/10.3390/vaccines10020163.

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Анотація:

Immune checkpoint inhibitors such as monoclonal antibodies (mAbs) are amongst the most important breakthroughs in cancer therapeutics. However, high cost and short acting time limits its affordability and clinical application. Therefore, an economical and durable alternative is urgently needed. Previously, we identified an IL-17RB targeting mAb which intercepts IL-17B/IL-17RB signal transduction and suppresses tumorigenesis in many types of cancer. We reason that active immunity against the antigenic epitope of IL-17RB can reproduce the anti-cancer effect of mAbs with better sustainability. Here, we present a cancer vaccine composed of multiple synthesized epitope peptides chemically conjugated onto CRM197, a highly immunogenic carrier protein. Combining mass spectrometry with immunoassay, we standardized hapten density determination and optimized vaccine design. Furthermore, orthotopically transplanted syngeneic mouse tumor 4T1 showed that administration of this vaccine therapeutically mitigates primary cancer growth as well as distance metastasis. In conclusion, we demonstrate preparation, characterization and pre-clinical application of a novel peptide cancer vaccine.

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Hossain, Awlad, Bevra Hahn, and Ram Singh. "Expression of interferon-inducible genes is influenced by sex hormones and gender in SLE (P1380)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 203.7. http://dx.doi.org/10.4049/jimmunol.190.supp.203.7.

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Abstract Women may be more susceptible than men to SLE and other autoimmune diseases in part because many healthy women have higher interferon regulated genes and fewer regulatory T cells. Similarly, female BWF1 lupus mice have increased expression of interferon genes compared to age and sex- matched males. Estradiol regulates interferon-inducible genes differentially in healthy controls and in SLE, with higher induction of IFN-inducible genes in the SLE population. Plasma 17b-estradiol levels are significantly increased in female SLE patients compared to healthy females (p<0.01). Testosterone (100 pg/ml) significantly increased FoxP3 expression in CD4+CD25+hi cells from women with SLE (p< 0.03). Estradiol increases proinflammatory cytokines and positively correlated with plasma levels of IL-6/ IL-21 and miR21, miR25 and miR186.

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Soares, Marcos, Gabriela Gomes Mânica, and Thiago Gomes Heck. "BIOMARCADORES NA RINITE ALÉRGICA: QUAL A IMPORTÂNCIA E POTENCIAL DIAGNÓSTICO?" Saúde e Pesquisa 10, no. 1 (July 21, 2017): 181. http://dx.doi.org/10.17765/1983-1870.2017v10n1p181-189.

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O objetivo deste estudo é apontar quais os novos potenciais marcadores biológicos na rinite alérgica (RA). Buscou-se nas bases de dados Scielo e PUBMED artigos com os descritores “Rinite Alérgica” e “Biomarcadores” ou “Citocinas” ou “Interleucinas” ou “Eicosanoides”, bem como na língua inglesa. A perspectiva do uso de novos biomarcadores na rinite alérgica vem sendo pesquisada, visto que marcadores sensíveis e específicos da doença poderiam permitir rápido diagnóstico, avaliação do estágio da doença e estimação da resposta ao tratamento. Vários métodos para coleta de amostras não invasivos ou semi-invasivos nas vias aéreas oferecem a possibilidade de mensuração de uma grande quantidade de novos biomarcadores na RA. Como potenciais biomarcadores, a análise do perfil de citocinas nasais apresenta uma boa caracterização diagnóstica (IL-5 e IL-13), além da relação de severidade da doença (IL-9 e IL-17B). Como avaliação isolada, a dosagem sérica de Proteína da Célula de Clara (CC16) parece ter grande potencial, pois permite o diagnóstico e seus níveis estão inversamente relacionados com a severidade da doença. Além disso, a dosagem de FeNO vem como uma arma importante para predizer asma nos pacientes com RA.

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Gangur, Venugopal, Yining Jin, Perry KW Ng, and Eric Olson. "An adjuvant-free mouse model of anaphylaxis to saline-soluble wheat protein." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 104.1. http://dx.doi.org/10.4049/jimmunol.200.supp.104.1.

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Abstract Wheat is a major food that can trigger life-threatening systemic anaphylaxis. Mechanism of sensitization to wheat anaphylaxis is not completely understood at present. For example, whether or not skin exposure to saline-soluble wheat protein (SSWP) can cause sensitization is unknown. Here we tested the hypothesis that transdermal exposure (TDE) to SSWP from durum wheat results in IgE response and clinical sensitization for anaphylaxis. Groups of Balb/c mice weaned onto a plant free diet received six TDEs with SSWP (1 mg/mouse/week) or saline over a 6 week period without adjuvant. Blood was analyzed for IgE responses by ELISA, and anaphylaxis and mucosal mast cell protease (mMCP-1) release upon challenge were quantified. Spleen tissue was analyzed for cytokines using a protein microarray system. Results showed significant IgE response, hypothermia shock response and elevation of mMCP-1 upon challenge. Spleen analysis showed significant elevations of IL-4/5/7/10/17B,E,F, and TSLP and significant reductions of IL-1a and IL-6. The following cytokines were not significantly altered: IL-1b/2/9/13/17A/22/23, IFNg and TNFa.

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Jackson, Shawn, Ada Undieh, Harold Steiner, Zuly Parra, Robert Miller, Yuko Ohta та Martin Flajnik. "Ontogenic analysis of Xenopus γδ T cells: expressed T cell receptor (TCR) γ and δ chains and IL-17 family members (160.8)". Journal of Immunology 188, № 1_Supplement (1 травня 2012): 160.8. http://dx.doi.org/10.4049/jimmunol.188.supp.160.8.

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Abstract γδ TCR that have structural differences from conventional γδ TCR in mammals have been observed in non-eutherian vertebrates. Three different types of Vδ regions are present in Xenopus tropicalis, similar to Vδ, Vα, and VHδ (derived from the V regions of Ig H chains). Semi-quantitative PCR analyses in adult and larval Xenopus laevis show that expression levels of TCRδC and TCRγC, as well as of TCRδV and TCRγV repertoires, vary between tissues. Comparative analyses of adult and larval CDR3 sequences suggest ontogenic-, tissue- and perhaps V family-specific expression. We have detected changes at the VDJ junctions including N-nucleotide addition, nucleotide trimming, and homologous recombination events. γδ T cell populations in mammals differentially express either IL-17 or IFNγ. In mammals, six IL-17 forms have been described (A-E), the least well characterized of which is IL-17D. Most non-mammalian IL-17 homologs, including those in chicken, fish, lamprey, nematode, oyster, sea urchin, and tunicate, and especially, Xenopus, are the IL-17D form. We have cloned two types of IL-17A/F, IL-17B, and IL-17D from X. laevis. Semi-quantitative PCR analyses in adult and larval Xenopus show that the expression of these IL-17 family members vary during ontogeny and between tissues. Study of γδ TCR and IL-17 family expression in Xenopus will illuminate evolutionary and developmental changes in γδ T cell antigen recognition and effector strategies.

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Laprevotte, Emilie, Stéphanie Cochaud, Stanislas du Manoir, Marion Lapierre, Cécile Dejou, Marion Philippe, Jérome Giustiniani, et al. "The IL-17B-IL-17 receptor B pathway promotes resistance to paclitaxel in breast tumors through activation of the ERK1/2 pathway." Oncotarget 8, no. 69 (December 6, 2017): 113360–72. http://dx.doi.org/10.18632/oncotarget.23008.

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34

Li, Jiahui, Yue Zhao, Marie Popp, Xiaolin Wu, Jie Qin, Jiangang Zhao, Zhefang Wang, et al. "Tumor-stroma metabolic symbolism via the IL-17B/RB axis affects metastatic potential of pancreatic ductal adenocarcinoma." Pancreatology 19 (June 2019): S83. http://dx.doi.org/10.1016/j.pan.2019.05.218.

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35

Gelaleti, Gabriela Bottaro, Thaiz Ferraz Borin, Larissa Bazela Maschio-Signorini, Marina Gobbe Moschetta, Bruna Victorasso Jardim-Perassi, Guilherme Berto Calvinho, Mariana Castilho Facchini, Alicia M. Viloria-Petit, and Debora Aparecida Pires de Campos Zuccari. "Efficacy of melatonin, IL-25 and siIL-17B in tumorigenesis-associated properties of breast cancer cell lines." Life Sciences 183 (August 2017): 98–109. http://dx.doi.org/10.1016/j.lfs.2017.06.013.

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36

Li, Jiahui, Yue Zhao, Christopher Betzler, Marie Popp, Jiangang Zhao, Qiye Sun, Judith Lohmann, et al. "The interaction of tumor and stroma via the IL-17B/RB axis affects metastatic potential of pancreatic ductal adenocarcinoma." Pancreatology 18, no. 4 (June 2018): S154. http://dx.doi.org/10.1016/j.pan.2018.05.414.

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Ge, Qian, Laurence Ryken, Laurence Noel, Eléonore Maury, and Sonia M. Brichard. "Adipokines identified as new downstream targets for adiponectin: lessons from adiponectin-overexpressing or -deficient mice." American Journal of Physiology-Endocrinology and Metabolism 301, no. 2 (August 2011): E326—E335. http://dx.doi.org/10.1152/ajpendo.00153.2011.

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Adipokines play a central role in the pathogenesis of the metabolic syndrome. Among them, adiponectin (ApN), a master regulator of immune and fuel homeostasis, is decreased. Identifying downstream adipokines targeted by ApN may help in deciphering this syndrome. We have generated transgenic mice, allowing persistent and moderate overexpression of ApN (ApN-Overex) specifically in white adipose tissue (AT). We took advantage of this model to unravel the adipokine secretion profile triggered by ApN. AT was fractionated into adipocytes and stromal-vascular cells (SVC), which were cultured for 8 h. Profiling of secretory products by antibody arrays and subsequent ELISAs showed that the secretion of three proinflammatory factors (IL-17B, IL-21, TNFα) and three hematopoietic growth factors [GF; thrombopoietin and granulocyte (macrophage) colony-stimulating-factors] was reduced in adipocytes of ApN-Overex mice compared with wild-type mice. In the SVC of these mice, besides the hematopoietic GFs, the secretion of another GF (vascular endothelial GF receptor 1), two chemokines (RANTES and ICAM-1), and two proinflammatory factors (IL-6 and IL-12p70) was reduced as well. Only one cytokine, IL-1 receptor 4, was oversecreted by SVC of ApN-Overex mice, which may exhibit anti-inflammatory properties. Most of these changes in secretion were due to corresponding changes in mRNAs. A reverse profile of adipokine expression was observed in ApN-KO mice. In conclusion, ApN regulates in vivo the secretion of downstream adipokines, thereby inducing a shift of the immune balance in both adipocytes and SVC toward a less inflammatory phenotype. These downstream adipokines may be new therapeutic targets for the management of the metabolic syndrome.

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Shokrollahi Barough, M., P. Fatemeh, K. Parviz, B. Mehdi, and F. Leila. "The supernatant of high metastatic breast cancer cell lines can change the IL-17B and MMP1 expression of breast non-malignant cells." European Journal of Cancer 92 (April 2018): S139. http://dx.doi.org/10.1016/s0959-8049(18)30640-3.

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Moore, Emma E., Scott Presnell, Ursula Garrigues, Angele Guilbot, Eric LeGuern, Deborah Smith, Lena Yao, et al. "Expression of IL-17B in neurons and evaluation of its possible role in the chromosome 5q-linked form of Charcot–Marie–Tooth disease." Neuromuscular Disorders 12, no. 2 (February 2002): 141–50. http://dx.doi.org/10.1016/s0960-8966(01)00250-4.

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Johanson, Gunnar, Aishwarya Mishra Dwivedi, Lena Ernstgård, Lena Palmberg, Koustav Ganguly, Lung Chi Chen, Karen Galdanes, Terry Gordon, and Swapna Upadhyay. "Analysis of Acrolein Exposure Induced Pulmonary Response in Seven Inbred Mouse Strains and Human Primary Bronchial Epithelial Cells Cultured at Air-Liquid Interface." BioMed Research International 2020 (October 8, 2020): 1–13. http://dx.doi.org/10.1155/2020/3259723.

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Background. Acrolein is a major component of environmental pollutants, cigarette smoke, and is also formed by heating cooking oil. We evaluated the interstrain variability of response to subchronic inhalation exposure to acrolein among inbred mouse strains for inflammation, oxidative stress, and tissue injury responses. Furthermore, we studied the response to acrolein vapor in the lung mucosa model using human primary bronchial epithelial cells (PBEC) cultured at an air-liquid interface (ALI) to evaluate the findings of mouse studies. Methods. Female 129S1/SvlmJ, A/J, BALB/cByJ, C3H/HeJ, C57BL/6J, DBA/2J, and FVB/NJ mice were exposed to 1 part per million (ppm) acrolein or filtered air for 11 weeks. Total cell counts and protein concentrations were measured in bronchoalveolar lavage (BAL) fluid to assess airway inflammation and membrane integrity. PBEC-ALI models were exposed to acrolein vapor (0.1 and 0.2 ppm) for 30 minutes. Gene expression of proinflammatory, oxidative stress, and tissue injury-repair markers was assessed (cut off: ≥2 folds; p < 0.05 ) in the lung models. Results. Total BAL cell numbers and protein concentrations remained unchanged following acrolein exposure in all mouse strains. BALB/cByJ, C57BL/6J, and 129S1/SvlmJ strains were the most affected with an increased expression of proinflammatory, oxidative stress, and/or tissue injury markers. DBA/2J, C3H/HeJ, A/J, and FVB/NJ were affected to a lesser extent. Both matrix metalloproteinase 9 (Mmp9) and tissue inhibitor of metalloproteinase 1 (Timp1) were upregulated in the strains DBA/2J, C3H/HeJ, and FVB/NJ indicating altered protease/antiprotease balance. Upregulation of lung interleukin- (IL-) 17b transcript in the susceptible strains led us to investigate the IL-17 pathway genes in the PBEC-ALI model. Acrolein exposure resulted in an increased expression of IL-17A, C, and D; IL-1B; IL-22; and RAR-related orphan receptor A in the PBEC-ALI model. Conclusion. The interstrain differences in response to subchronic acrolein exposure in mouse suggest a genetic predisposition. Altered expression of IL-17 pathway genes following acrolein exposure in the PBEC-ALI models indicates that it has a central role in chemical irritant toxicity. The findings also indicate that genetically determined differences in IL-17 signaling pathway genes in the different mouse strains may explain their susceptibility to different chemical irritants.

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Bridges, Phillip J., Myoungkun Jeoung, Sarah Shim, Ji Yeon Park, Jae Eun Lee, Lindsay A. Sapsford, Kourtney Trudgen, Chemyong Ko, Myung Chan Gye, and Misung Jo. "Hematopoetic Prostaglandin D Synthase: An ESR1-Dependent Oviductal Epithelial Cell Synthase." Endocrinology 153, no. 4 (February 28, 2012): 1925–35. http://dx.doi.org/10.1210/en.2011-1900.

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Oviductal disease is a primary cause of infertility, a problem that largely stems from excessive inflammation of this key reproductive organ. Our poor understanding of the mechanisms regulating oviductal inflammation restricts our ability to diagnose, treat, and/or prevent oviductal disease. Using mice, our objective was to determine the spatial localization, regulatory mechanism, and functional attributes of a hypothesized regulator of oviductal inflammation, the hematopoietic form of prostaglandin D synthase (HPGDS). Immunohistochemistry revealed specific localization of HPGDS to the oviduct's epithelium. In the isthmus, expression of HPGDS was consistent. In the ampulla, expression of HPGDS appeared dependent upon stage of the estrous cycle. HPGDS was expressed in the epithelium of immature and cycling mice but not in the oviducts of estrogen receptor α knockouts. Two receptor subtypes bind PGD2: PGD2 receptor and G protein-coupled receptor 44. Expression of mRNA for Ptgdr was higher in the epithelial cells (EPI) than in the stroma (P < 0.05), whereas mRNA for Gpr44 was higher in the stroma than epithelium (P < 0.05). Treatment of human oviductal EPI with HQL-79, an inhibitor of HPGDS, decreased cell viability (P < 0.05). Treatment of mice with HQL-79 increased mRNA for chemokine (C-C motif) ligands 3, 4, and 19; chemokine (C-X-C motif) ligands 11 and 12; IL-13 and IL-17B; and TNF receptor superfamily, member 1b (P < 0.02 for each mRNA). Overall, these results suggest that HPGDS may play a role in the regulation of inflammation and EPI health within the oviduct.

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Gangur, Venugopal, Yining Jin, Haoran Gao, Rick Jorgensen, and Perry KW Ng. "Immune-markers for assessment of wheat allergenicity in mice: comparison of adjuvant-free vs. alum-adjuvant based models." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 55.6. http://dx.doi.org/10.4049/jimmunol.202.supp.55.6.

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Abstract Immediate hypersensitivity reaction to wheat proteins is a major type of food allergy in many countries including the USA. Mechanisms of wheat allergenicity are incompletely understood at present. Reliable and validated in vivo immune-markers for assessment of allergenicity potential of different wheat products are unavailable at present. Published mouse models of wheat allergy have mostly used adjuvants to induce wheat allergenicity. However, it is not clear whether such models are useful to develop reliable immune-markers to assess allergenicity of different wheat products. Here we compared the immune-markers of allergenicity between an adjuvant-free transdermal exposure (TDE) model and an alum-adjuvant (AA) mouse model of anaphylaxis induced by salt-soluble wheat protein (SSWP) extract. In the TDE model, Balb/cJ mice were sensitized with SSWP by six weekly exposures. In the AA model, mice were sensitized by intraperitoneal injection of SSWP with alum. In both models, significant IgE as well as MMCP-1 responses were elicited. Analysis of spleen immune-markers using a quantibody multiplex assay, identified IL-4, -5, -17B/E, -20, CCL4,5,11, CXCL4, and CD40L as useful markers in the TDE model. In the AA model, with the exception of IL-5 and -13, none of the immune-markers tested were found useful. Our data demonstrate that the TDE model is better than the AA model for development of in vivo immune-markers for assessment of wheat protein allergenicity. Funding: USDA, National Institute of Food and Agriculture, Hatch project MICL02486 (Accession Number: 1012322) and Agricultural and Food Research Initiative Competitive Program#2018-67017-27876; Michigan State University/FSHN.

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Chen, Yiwen, Yan Xiong, Jun Luo, Qianchao Hu, Jianan Lan, Yongkang Zou, Qin Ma та ін. "Aldehyde Dehydrogenase 2 Protects the Kidney from Ischemia–Reperfusion Injury by Suppressing the IκBα/NF-κB/IL-17C Pathway". Oxidative Medicine and Cellular Longevity 2023 (21 лютого 2023): 1–16. http://dx.doi.org/10.1155/2023/2264030.

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Objective. Ischemia–reperfusion injury (IRI) is an important cause of delayed functional recovery after transplantation. This study is aimed at investigating the molecular mechanism of ALDH2 in a kidney ischemia–reperfusion model based on RNA-seq. Methods. We performed kidney ischemia–reperfusion in ALDH2-/- and WT mice and evaluated kidney function and morphology using SCr, HE staining, TUNEL staining, and TEM. We used RNA-seq to compare mRNA expression in ALDH2-/- and WT mice after IR, and then, we verified the related molecular pathways by PCR and western blotting. In addition, activators and inhibitors of ALDH2 were used to alter the activity of ALDH2. Finally, we established a model of hypoxia and reoxygenation in HK-2 cells and clarified the role of ALDH2 in IR by interfering with ALDH2 and using an NF-κB inhibitor. Results. After kidney ischemia–reperfusion, the SCr value increased significantly, kidney tubular epithelial cells were damaged, and the apoptosis rate increased. In the microstructure, mitochondria were swollen and deformed, and ALDH2 deficiency aggravated these changes. The NF-κB pathway and IL-17 pathway were significantly enriched in ALDH2-/- mice compared with WT mice according to KEGG enrichment analysis of the RNA-seq data. The PCR results showed that the mRNA expression levels of IκBα and IL-17B, C, D, E, and F were significantly higher than those in the WT-IR group. Western blot verification results showed that ALHD2 knockdown resulted in increased phosphorylation of IκBα, increased phosphorylation of NF-κB, and increased expression of IL-17C. When we used ALDH2 agonists, the number of lesions and the expression levels of the corresponding proteins were reduced. Knockdown of ALDH2 in HK-2 cells resulted in a higher proportion of apoptotic cells after hypoxia and reoxygenation, but inhibiting the phosphorylation of NF-κB prevented the increase in apoptosis and reduced the protein expression level of IL-17C. Conclusion. ALDH2 deficiency can lead to the aggravation of kidney ischemia–reperfusion injury. RNA-seq analysis and validation by PCR and western blotting revealed that this effect may be due to the promotion of IκBα/NF-κB p65 phosphorylation during ischemia–reperfusion caused by ALDH2 deficiency, which then leads to an increase in inflammatory factors, including IL-17C. Thus, cell death is promoted, and kidney IRI is eventually aggravated. We link ALDH2 deficiency with inflammation, revealing a new idea for ALDH2-related research.

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Dinesh, Ravi, Bevra Hahn, and Ram Singh. "Sex hormones and gender influence the expression of Foxp3 and regulatory T cells in SLE patients (115.18)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 115.18. http://dx.doi.org/10.4049/jimmunol.186.supp.115.18.

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Abstract Regulatory T cells have been implicated in the maintenance of immune tolerance. Whether sex hormones and gender influence the expression of FoxP3 and regulatory T cells remain obscure. We provide the first evidence in this study that numbers and percent expression of regulatory T cells are significantly reduced in healthy females compared to healthy males. We found that both CD4+CD25+hi and CD8+CD25hi+ subsets of healthy males had 3-4-fold higher Foxp3 mRNA compared to healthy females. Estrogen increases proinflammatory cytokines and plasma estradiol positively correlated with IL-21 in SLE pts. Levels of estradiol positively correlated with SLEDAI score. Testosterone level was decreased in SLE women compared to healthy women. Furthermore, testosterone significantly increased FoxP3 expression in CD4+CD25hi cells from women with SLE. Plasma concentrations of testosterone positively correlated with the expression of FoxP3 in Treg. These data demonstrate that women may be more susceptible than men to SLE and other autoimmune diseases in part because many healthy women have fewer regulatory T cells and less FoxP3 expression. In addition, women with SLE, compared to healthy women, seem to have less ability to generate CD4+ Treg in response to physiologic concentrations of 17b-estradiol, whereas testosterone metabolite increases the generation of Tregs. These data suggest that gender and sex hormones influence susceptibility to SLE via their effects on Treg and Foxp3 expression.

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Siebert, S., I. Mcinnes, M. J. Loza, K. MA, K. Leander, V. Lakshminarayanan, C. Franks, P. Cooper, and K. Sweet. "OP0229 GUSELKUMAB INDUCES SUSTAINED REDUCTION IN ACUTE PHASE PROTEINS AND TH17 EFFECTOR CYTOKINES IN ACTIVE PSORIATIC ARTHRITIS IN TWO PHASE-3 CLINICAL TRIALS (DISCOVER-1 AND DISCOVER-2)." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 144–45. http://dx.doi.org/10.1136/annrheumdis-2020-eular.1240.

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Background:Guselkumab (GUS), an IL-23 inhibitor monoclonal antibody (Mab) that specifically binds to the IL-23p19 subunit, demonstrated efficacy compared to placebo (PBO) in reducing skin and musculoskeletal signs and symptoms in patients (pts) with active psoriatic arthritis (PsA) in two phase-3 studies, DISCOVER 1 & 2.1,2Previous results from a GUS PsA Phase-2 trial3and Ustekinumab (UST, anti-IL12/23p40 MAb) PsA Phase-3 trials (PSUMMIT 1 & 2)4showed associations of baseline IL-17A, IL-17F, and CRP with baseline disease characteristics, and associations of GUS-induced cytokine reductions with clinical responses.Objectives:To investigate plausible cytokine expression in PsA and alterations after exposure to GUS therapy.Methods:In DISCOVER 1 & 2, pts were treated with GUS 100 mg at Wk 0, 4, then every 8Wks (q8w); GUS 100mg q4w; or matching PBO. 21 serum biomarkers were measured in a random subset of 300 PsA pts from the DISCOVER program at Weeks (Wks) 0, 4, & 24 and in 34 healthy controls matched for age, sex, and ethnicity. Serum proteins measured were acute phase reactants CRP & SAA (Meso Scale Discovery (MSD) Platform) and inflammatory cytokines/chemokines: Th17 effector cytokines IL-17A, IL-17F, & IL-22 (Single Molecule Counting Erenna® Immunoassay Platform) and soluble ICAM-1, soluble VCAM-1, IL-6, CXCL-8, IL-10, IL-13, IL-12p70, CCL22, IFN-γ, CCL2, CCL4, TNFα, IL-1β, IL-2, IL-4 (MSD), & YKL-40 (Quantikine Immunoassay). Serum IL-17A, IL-17B, & CRP measured in the Phase-3 PSUMMIT trials of UST for PsA4were included for comparison with GUS.Results:At baseline, serum levels of acute phase proteins CRP, SAA, & IL-6, and Th17-effector cytokines IL-17A & IL-17F were elevated in pts with PsA compared with healthy controls (p<0.05, geometric mean ≥ 40% higher, FIG 1). There was no significant dysregulation in the other cytokines measured in PsA pts compared to healthy controls. Baseline IL-17A, IL-17F, IL-22, & CCL22 were significantly associated with baseline psoriasis disease activity (Body Surface Area & Psoriatic Area and Severity Index, Spearman Signed Rank p<0.05, r>0.25). Baseline CRP, SAA, IL-6, & YKL40 were significantly associated with baseline joint disease (Disease Activity Score 28-CRP, Spearman p<0.05, r>0.25). Baseline SAA, IL-6, IL-17A, & IL-17F were higher in pts with prior TNF inhibitor exposure than without (p<0.05, geometric mean ≥ 40% higher), although pts with PsA both with and without prior TNF inhibitor had higher levels than the healthy control set.GUS treatment resulted in decreases in serum CRP, SAA, IL-6, IL-17A, IL-17F, & IL-22 that were significantly greater than PBO as early as Week 4 (FIG 1). These protein levels continued to decrease through Wk 24 in GUS-treated pts with both dosing regimens (p<0.05, geometric mean decrease from baseline ≥ 33%). Further, Wk 24 IL-17A & IL-17F levels for pts treated with either dose of GUS were not significantly different from healthy controls, suggesting a normalization of peripheral effector cytokines associated with the IL-23/Th17 axis following treatment with GUS. Effects on IL-17A/IL-17F were greater in GUS treated pts than UST treated pts, while CRP levels were similar in both programs (FIG 2).Conclusion:Comprising a strong pharmacodynamic effect, GUS treatment reduced serum protein levels of acute phase and Th17-effector cytokines (whose elevations at baseline were associated with PsA disease characteristics) and achieved comparable levels to those in healthy controls. In pts with PsA, reductions of IL-17A and IL-17F by GUS were of greater magnitude than those by UST.References:[1]Deodhar et al. ACR 2019, abs #807. Arth Rheumatol. 2019;71 S10: 1386[2]Mease et al. ACR 2019, abs #L13. Arth Rheumatol. 2019;71 S10:5247[3]Siebert et al. EULAR 2019, abs #479. Ann Rheum Dis. 2019;78 S2:293[4]Siebert et al. Arth Rheumatol. 2019;71:1660Acknowledgments:NoneDisclosure of Interests:Stefan Siebert Grant/research support from: BMS, Boehringer Ingelheim, Celgene, GlaxoSmithKline, Janssen, Novartis, Pfizer, UCB, Consultant of: AbbVie, Boehringer Ingelheim, Janssen, Novartis, Pfizer, UCB, Speakers bureau: AbbVie, Celgene, Janssen, Novartis, Iain McInnes Grant/research support from: Bristol-Myers Squibb, Celgene, Eli Lilly and Company, Janssen, and UCB, Consultant of: AbbVie, Bristol-Myers Squibb, Celgene, Eli Lilly and Company, Gilead, Janssen, Novartis, Pfizer, and UCB, Matthew J Loza Employee of: Janssen Research & Development, LLC, Keying Ma Employee of: Janssen Research & Development, LLC, Karen Leander, Employee of: Janssen Research & Development, LLC, Vani Lakshminarayanan Employee of: Janssen Research & Development, LLC, Carol Franks Employee of: Janssen Research & Development, LLC, Philip Cooper Employee of: Janssen Research & Development, LLC, Kristen Sweet Employee of: Janssen Research & Development, LLC

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Liszewska, Agata, Ewa Robak, Anna Woźniacka, Jaroslaw Bogaczewicz, Bożena Dziankowska-Bartkowiak, and Zofia Gerlicz-Kowalczuk. "Interplay between IL-17 family members and angiogenic cytokines in subjects with systemic sclerosis." Archives of Medical Science, March 21, 2021. http://dx.doi.org/10.5114/aoms/128102.

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IntroductionSystemic sclerosis (SSc) is a chronic, autoimmune connective tissue disease characterized by immune system activation, vasculopathy, and collagen accumulation. Despite progressive fibrosis of the vasculature, compensatory angiogenesis is impaired. The cause of the shift towards anti-angiogenesis observed in SSc is unknown. The IL-17 cytokine family participates in the pathogenesis of SSc and angiogenesis.Material and methodsOur study aimed to evaluate levels and find relationships between the levels of proangiogenic cytokines and cytokines from the IL-17 family in 42 SSc subjects and 20 healthy controls. VEGF, PlGF, HGF, TGFβ1, GM-CSF, IL-17A, IL-17B, IL-17E and IL-17F were quantified in the sera of all participants by ELISA sandwich kits.ResultsSignificantly higher mean concentrations of PlGF compared to controls - mean value (19.3 pg/ml in the SSc group vs. 11.4 pg/ml in the control group; p<0.001) and of HGF (1931 pg/ml in the SSc group vs. 1483 pg/ml in controls; p<0.05). Mean serum TGFβ1 level was also significantly lower in the SSc group (781 pg/ml) than controls (35991 pg/ml; p<0.001). Among the IL-17 family, significantly higher mean concentrations of IL-17B (67.0 pg/ml vs. 2.6 pg/ml in controls; p<0,001), IL-17E (8.0 pg/ml vs 0.64 pg/ml in controls; p<0.001) and IL-17F (0.42 pg/ml vs. 0.0 pg/ml in controls; p< 0.01) were detected. Serum concentrations of HGF and PlGF correlated with the concentrations of IL17A, IL-17B, and IL-17E.ConclusionsIn conclusion, our findings indicate that selected cytokines from the IL17 family participate in the pathogenesis of SSc and are responsible for the vascular abnormalities associated with this disorder.

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Bastid, Jérémy, Cécile Dejou, Aurélie Docquier, and Nathalie Bonnefoy. "The Emerging Role of the IL-17B/IL-17RB Pathway in Cancer." Frontiers in Immunology 11 (April 21, 2020). http://dx.doi.org/10.3389/fimmu.2020.00718.

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48

Tawalbeh, Shefa M., Wilfredo Marin, Gabrielle A. Morgan, Utkarsh J. Dang, Yetrib Hathout, and Lauren M. Pachman. "Serum protein biomarkers for juvenile dermatomyositis: a pilot study." BMC Rheumatology 4, no. 1 (October 1, 2020). http://dx.doi.org/10.1186/s41927-020-00150-7.

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Abstract Background Blood accessible biomarkers to assess disease activity and their response to therapies in Juvenile Dermatomyositis (JDM) are urgently needed. This pilot study aims to identify serum protein biomarkers associated with clinical disease activity in untreated JDM and their response to medical therapy. Methods SomaScan® technology screened JDM patients for 1305 proteins at three points: 1) before start of treatment, 2) while on therapy, and 3) after treatment tapering when patients were clinically inactive. To define disease associated biomarkers, SomaScan® data from untreated JDM patients (n = 8) were compared to SomaScan® data from an independent age-matched healthy control group (n = 12). Longitudinal analysis defined treatment responsive proteins at three time points: untreated (7 samples), treated (7 samples), and clinically inactive (6 samples). To confirm the SomaScan® data, a subset of nine candidate proteins (CXCL11, IL-17B, IL-17D, IL-22, CXCL10, MCP-1, ANGPT2, MIF, IL-23) were tested by ELISA after adding 2 JDM (one untreated, one clinically inactive) serum samples to the same group of JDM girls (8 untreated, 7 treated; 7 clinically inactive) as well as with 17 age, gender, matched healthy controls. Results Comparison of untreated JDM versus healthy controls identified 202 elevated and 49 decreased serum proteins in JDM patients with an adjusted p-value < 0.001. Only 82 out of 251 identified biomarker candidates responded to treatment while 12 out of these 82 proteins returned to their original untreated disease levels upon therapy tapering. The ELISA testing of the untreated samples for nine candidate proteins confirmed previously known biomarkers (CXCL10 or IP-10, CXCL11 or I-TAC and MCP-1) and identified novel biomarkers including IL-22, Angiopoetin-2, and IL-17B in a cross-sectional analysis comparing 8 untreated JDM and 17 age/gender matched controls. The subsequent longitudinal data by ELISA were not concordant for some biomarkers (IL-22 and IL-17B), but the other biomarkers either normalized or rebounded concordantly. Conclusions Blood accessible protein biomarkers reflecting JDM pathophysiology were identified; some of them rebounded after therapy was tapered. Further studies bridging these biomarkers to specific clinical features of JDM are required to confirm the clinical utility of these serum protein biomarkers.

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Bottaro Gelaleti, G., C. Leonel, BV Perassi-Jardim, LC Ferreira, MG Moschetta, TF Borin, LB Maschio, GR Martins, AM Viloria-Petit, and DAPC Zuccari. "P62. Effectiveness of melatonin, IL-25 and siRNA IL-17B in growth control of breast cancer cell lines." Journal for ImmunoTherapy of Cancer 2, S2 (March 2014). http://dx.doi.org/10.1186/2051-1426-2-s2-p36.

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Butcher, Matthew J., and Elena V. Galkina. "Abstract 552: IL-17C-Producing Aortic Smooth Muscle Cells Play a Pro-Atherogenic Role Via the Recruitment of Inflammatory IL-17A+ T Cells." Arteriosclerosis, Thrombosis, and Vascular Biology 35, suppl_1 (May 2015). http://dx.doi.org/10.1161/atvb.35.suppl_1.552.

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Atherosclerosis is characterized by frequent communication between infiltrating leukocytes and vascular cells, through chemokine and cytokine networks. Various IL-17 cytokine family members are detected within atherosclerotic plaques; however the involvement of IL-17B-IL-17E has not been thoroughly examined. Aortic IL-17 cytokines were initially profiled and Il17a, Il17f, and Il17c mRNA expression was found to be elevated in Apoe-/- aortas in comparison to C57Bl6 controls. To determine the cellular sources of aortic IL-17C, aortic IL-17C-producing cells were phenotyped by flow cytometry. Surprisingly, these experiments revealed a major population of IL-17C-producing smooth muscle cells within Apoe-/- versus C57Bl6 aortas. To determine the role of IL-17C in atherosclerosis, we generated Il17c-/-Apoe-/- mice and compared 12 week western diet-fed Apoe-/- and Il17c-/-Apoe-/- mice. Atherosclerotic lesions were reduced by 42±2.6% in WD-fed Il17c-/-Apoe-/- aortas in comparison to Apoe-/- controls. Flow cytometric analyses of Il17c-/-Apoe-/- mice revealed a reduction in the number of aortic leukocytes, macrophages, neutrophils, and T cells, which corresponded with smaller atherosclerotic lesions (40±5%). However, the percentage and number of aortic IL-17A+ TCRγδ T cells and Th17 cells were disproportionately reduced within Il17c-/-Apoe-/- aortas (70±5%). We hypothesized that IL-17C might support the recruitment of Th17 cells to the aorta. To study comparative Th17 migration, Apoe-/- T cells were transferred to western diet-fed Il17c-/-Apoe-/- and Apoe-/- recipients and examined for Th1 and Th17 migration 48 hours post transfer. We found diminished accumulation of Th17, but not Th1 T cells, in the aortas of Il17c-/-Apoe-/- versus Apoe-/- recipients. Thus smooth muscle cell-derived IL-17C plays a pro-atherogenic role by supporting the recruitment of Th17 cells to atherosclerotic lesions.

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