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Literatura académica sobre el tema "IL-17F"

Autor: Grafiati

Publicado: 11 de marzo de 2023

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Artículos de revistas sobre el tema "IL-17F"

1

Wright, Jill F., Frann Bennett, Bilian Li, Jonathan Brooks, Deborah P. Luxenberg, Matthew J. Whitters, Kathleen N. Tomkinson et al. "The functional activity of human IL-17A, IL-17F and IL-17A/IL-17F cytokines is dependent on the receptors IL-17R and IL-17RC (94.31)". Journal of Immunology 178, n.º 1_Supplement (1 de abril de 2007): S176. http://dx.doi.org/10.4049/jimmunol.178.supp.94.31.

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Abstract IL-17A and IL-17F are members of the IL-17 cytokine family and have been detected in tissue samples from patients with autoimmune disease. Recent data has shown that these cytokines are secreted by a new CD4+ T cell lineage known as Th17 cells. We have recently demonstrated that activated human CD4+ T cells also produce the IL-17A/IL-17F heterodimer with in vitro functional activity. Both IL-17R and IL-17RC are required for activity of IL-17A and IL-17F. However, the question remains whether IL-17A/IL-17F also utilizes the same receptors for activity or whether it signals through different receptor chains. ELISA and BiaCore-based binding experiments were performed to determine if IL-17A/IL-17F could bind to IL-17R and IL-17RC. We find that IL-17A, IL-17F and IL-17A/IL-17F each bind to IL-17R but with different affinities, whereas they bind to IL-17RC with comparable affinity. Using cell based assays, we have evaluated the functional activity of IL-17A, IL-17F and IL-17A/IL-17F in the presence of soluble receptors, antibodies to the receptors and IL-17R and IL-17RC siRNA. We find that the activity of IL-17A, IL-17F and IL-17A/IL-17F is decreased when the expression of IL-17R is reduced, whereas the activity of the cytokines decreases to a lesser extent when the expression of IL-17RC is reduced. In conclusion, our results suggest that IL-17A, IL-17F and IL-17A/IL-17F each bind and signal through the same receptor complex.

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2

Yang, Xuexian O., Seon Hee Chang, Heon Park, Roza Nurieva, Bhavin Shah, Luis Acero, Yi-Hong Wang et al. "Regulation of inflammatory responses by IL-17F". Journal of Experimental Medicine 205, n.º 5 (14 de abril de 2008): 1063–75. http://dx.doi.org/10.1084/jem.20071978.

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Although interleukin (IL) 17 has been extensively characterized, the function of IL-17F, which has an expression pattern regulated similarly to IL-17, is poorly understood. We show that like IL-17, IL-17F regulates proinflammatory gene expression in vitro, and this requires IL-17 receptor A, tumor necrosis factor receptor–associated factor 6, and Act1. In vivo, overexpression of IL-17F in lung epithelium led to infiltration of lymphocytes and macrophages and mucus hyperplasia, similar to observations made in IL-17 transgenic mice. To further understand the function of IL-17F, we generated and analyzed mice deficient in IL-17F or IL-17. IL-17, but not IL-17F, was required for the initiation of experimental autoimmune encephalomyelitis. Mice deficient in IL-17F, but not IL-17, had defective airway neutrophilia in response to allergen challenge. Moreover, in an asthma model, although IL-17 deficiency reduced T helper type 2 responses, IL-17F–deficient mice displayed enhanced type 2 cytokine production and eosinophil function. In addition, IL-17F deficiency resulted in reduced colitis caused by dextran sulfate sodium, whereas IL-17 knockout mice developed more severe disease. Our results thus demonstrate that IL-17F is an important regulator of inflammatory responses that seems to function differently than IL-17 in immune responses and diseases.

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3

Almahmoudi, Rabeia, Abdelhakim Salem, Sakhr Murshid, Mauricio Rocha Dourado, Ehsanul Hoque Apu, Tuula Salo y Ahmed Al-Samadi. "Interleukin-17F Has Anti-Tumor Effects in Oral Tongue Cancer". Cancers 11, n.º 5 (11 de mayo de 2019): 650. http://dx.doi.org/10.3390/cancers11050650.

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We recently showed that extracellular interleukin-17F (IL-17F) correlates with better disease-specific survival in oral tongue squamous cell carcinoma (OTSCC) patients. However, the underlying mechanisms of such effect remain obscure. Here, we used qRT-PCR to assess the expression of IL-17F and its receptors (IL-17RA and IL-17RC) in two OTSCC cell lines (HSC-3 and SCC-25) and in normal human oral keratinocytes (HOKs). IL-17F effects on cancer cell proliferation, migration, and invasion were studied using a live-imaging IncuCyte system, and a Caspase-3/7 reagent was used for testing apoptosis. 3D tumor spheroids were utilized to assess the impact of IL-17F on invasion with or without cancer-associated fibroblasts (CAFs). Tube-formation assays were used to examine the effects of IL-17F on angiogenesis using human umbilical vein endothelial cells (HUVEC). OTSCC cells express low levels of IL-17F, IL-17RA, and IL-17RC mRNA compared with HOKs. IL-17F inhibited cell proliferation and random migration of highly invasive HSC-3 cells. CAFs promoted OTSCC invasion in tumor spheroids, whereas IL-17F eliminated such effect. IL-17F suppressed HUVEC tube formation in a dose-dependent manner. Collectively, we suggest that IL-17F counteracts the pro-tumorigenic activity in OTSCC. Due to its downregulation in tumor cells and inhibitory activity in in vitro cancer models, targeting IL-17F or its regulatory pathways could lead to promising immunotherapeutic strategies against OTSCC.

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4

Luo, Zhenhua, Hui Wang, Yunlong Wu, Zheng Sun y Yafei Wu. "Clinical Significance of IL-23 Regulating IL-17A and/or IL-17F Positive Th17 Cells in Chronic Periodontitis". Mediators of Inflammation 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/627959.

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Objective. To investigate the expression level and clinical significance of (IL-17A+and/or IL-17F+) Th17 cells under IL-23 regulation in patients of chronic periodontitis (CP) and healthy controls (HC).Materials and Methods. The whole peripheral blood samples were collected from 30 CP patients and 25 healthy controls. Flow cytometry was used to test the (IL-17A+and/or IL-17F+) Th17 expression level. Recombinant human IL-23 (rhIL-23) was used to detect Th17 differentiation and expansion. Correlation coefficient analysis between Th17 expression level and clinical parameters was analyzed by SPSS software.Results. Flow cytometry results showed that IL-17A+IL-17F−and IL-17A−IL-17F+Th17 were both increased in CP group than in HC group (P< 0.01), while, under recombinant human IL-23 (rhIL-23) stimulation, the number of IL-17A+IL-17F−Th17 cells was significantly increased in both CP and HC groups (P< 0.01). Interestingly, IL-17A−IL-17F+Th17 cells were only increased in CP group after rhIL-23 stimulation. Additionally, correlation coefficient analysis showed significant correlation between IL-17A+IL-17F−Th17 cell and attachment loss or probing depth (P< 0.05).Conclusions. This study indicates that both the IL-17A+IL-17F−and IL-17A−IL-17F+Th17 cells may be involved in pathogenesis of periodontitis. The role of these Th17 cells in the disease pathogenesis needs to be further investigated.

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5

Umemura, Masayuki, Masayuki Fukui, Chiho Fukui, Susumu Nakae, Yoichiro Iwakura y Goro Matsuzaki. "Role of IL-17 in chronic pulmonary mycobacterial infection. (MPF1P.775)". Journal of Immunology 192, n.º 1_Supplement (1 de mayo de 2014): 66.14. http://dx.doi.org/10.4049/jimmunol.192.supp.66.14.

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Abstract IL-17 family cytokine is comprised of six members, IL-17A to IL-17F. Recent studies using cytokine- and receptor-deficient mice showed that IL-17A and IL-17F were required for responses to extracellular bacterium K. pneumonia in the lungs and C. rodentium in the colon, respectively. However, the involvement of IL-17A and IL-17F in protective immunity was well not clearly demonstrated in mycobacterial infected lung. In this study, we analyzed role of IL-17A and IL-17F in host defense against chronically infected M. tuberculosis. using IL-17A- and IL-17F-KO mice. The IL-17A-KO mice showed significantly decreased survival rates compared with the wild-type (WT) mice during 250-day observation period. In contrast, survival rate of the IL-17F-KO mice were similar to that of the WT mice. Bacterial burdens of various organs of the IL-17F-KO mice on the day 250 were nearly the same as that in the WT mice. In the infected lungs, the IL-17A-KO mice produced less IFN-γ, TNF and IL-6 in comparison to those from the WT mice, while cytokine production of the IL-17F-KO mice were similar to that of the WT mice. This result indicated that the generation of Th1 cells was impaired in the IL-17A-KO mice but not in the IL-17F-KO mice infected with M. tuberculosis. These data strongly support the notion that the lack of IL-17F neither suppress nor enhances protective immunity in the lung after mycobacterial infection.

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6

Ota, Kyoko, Mio Kawaguchi, Satoshi Matsukura, Masatsugu Kurokawa, Fumio Kokubu, Junichi Fujita, Yuko Morishima et al. "Potential Involvement of IL-17F in Asthma". Journal of Immunology Research 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/602846.

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The expression of IL-17F is seen in the airway of asthmatics and its level is correlated with disease severity. Several studies have demonstrated that IL-17F plays a pivotal role in allergic airway inflammation and induces several asthma-related molecules such as CCL20. IL-17F-induced CCL20 may attract Th17 cells into the airway resulting in the recruitment of additional Th17 cells to enhance allergic airway inflammation. We have recently identified, for the first time, that bronchial epithelial cells are its novel cell source in response to IL-33 via ST2-ERK1/2-MSK1 signaling pathway. The receptor for IL-17F is the heterodimeric complex of IL-17RA and IL-17RC, and IL-17F activates many signaling pathways. In a case-control study of 867 unrelated Japanese subjects, a His161 to Arg161 (H161R) substitution in the third exon of the IL-17F gene was associated with asthma. In atopic patients with asthma, prebronchodilator baseline FEV1/FVC values showed a significant association with the H161R variant. Moreover, this variant is a natural antagonist for the wild-type IL-17F. Moreover, IL-17F is involved in airway remodeling and steroid resistance. Hence, IL-17F may play an orchestrating role in the pathogenesis of asthma and may provide a valuable therapeutic target for development of novel strategies.

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7

Kawaguchi, Mio, Junichi Fujita, Fumio Kokubu, Shau-Ku Huang, Tetsuya Homma, Satoshi Matsukura, Mitsuru Adachi y Nobuyuki Hizawa. "IL-17F-induced IL-11 release in bronchial epithelial cells via MSK1-CREB pathway". American Journal of Physiology-Lung Cellular and Molecular Physiology 296, n.º 5 (mayo de 2009): L804—L810. http://dx.doi.org/10.1152/ajplung.90607.2008.

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IL-17F is involved in asthma, but its biological function and signaling pathway have not been fully elucidated. IL-11 is clearly expressed in the airway of patients with allergic airway diseases such as asthma and plays an important role in airway remodeling and inflammation. Therefore, we investigated the expression of IL-11 by IL-17F in bronchial epithelial cells. Bronchial epithelial cells were cultured in the presence or absence of IL-17F and/or Th2 cytokines (IL-4 and IL-13) or various kinase inhibitors to analyze the expression of IL-11. Next, activation of mitogen- and stress-activated protein kinase (MSK) 1 by IL-17F was investigated. Moreover, the effect of short interfering RNAs (siRNAs) targeting MSK1 and cAMP response element binding protein (CREB) on IL-17F-induced IL-11 expression was investigated. IL-17F induced IL-11 expression, whereas the costimulation with IL-4 and IL-13 augmented this effect even further. MEK inhibitors PD-98059, U0126, and Raf1 kinase inhibitor I, significantly inhibited IL-11 production, whereas overexpression of a Raf1 dominant-negative mutant inhibited its expression. IL-17F clearly phosphorylated MSK1, whereas PD-98059 inhibited the phosphorylation of IL-17F-induced MSK1. Both MSK1 inhibitors Ro-31-8220 and H89 significantly blocked IL-11 expression. Moreover, transfection of the cells with siRNAs targeting MSK1 inhibited activation of CREB, and the siRNAs targeting MSK1 and CREB blocked expression of IL-11. These data suggest that IL-17F may be involved in airway inflammation and remodeling via the induction of IL-11, and RafI-MEK1/2-ERK1/2-MSK1-CREB is identified as a novel signaling pathway participating in this process. Therefore, the IL-17F/IL-11 axis may be a valuable therapeutic target for asthma.

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8

Nozato, Kyoko, Junichi Fujita, Mio Kawaguchi, Gen Ohara, Yuko Morishima, Yukio Ishii, Shau-Ku Huang, Fumio Kokubu, Hiroaki Satoh y Nobuyuki Hizawa. "IL-17F Induces CCL20 in Bronchial Epithelial Cells". Journal of Allergy 2011 (13 de octubre de 2011): 1–8. http://dx.doi.org/10.1155/2011/587204.

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IL-17F plays a crucial role in airway inflammatory diseases including asthma, but its function has not been fully elucidated. CCL20 is also involved in allergic airway inflammation, while its regulatory mechanisms remain to be defined. To further identify a novel role of IL-17F, the expression of CCL20 by IL-17F in bronchial epithelial cells and the signaling mechanisms involved were investigated. Bronchial epithelial cells were stimulated with IL-17F, and the levels of CCL20 gene and protein measured, with the effects of the addition of various kinase inhibitors and siRNAs also investigated. IL-17F significantly induced the expression of CCL20 gene and protein. Pretreatment with inhibitors for MEK1/2, Raf1 and MSK1, and overexpression of a Raf1 dominant-negative mutant significantly diminished IL-17F-induced CCL20 production. Moreover, transfection of the siRNAs targeting MSK1, p90RSK, and CREB blocked CCL20 expression. These findings suggest that IL-17F is able to induce CCL20 via Raf1-MEK1/2-ERK1/2-MSK1/p90RSK-CREB signaling pathway in bronchial epithelial cells. The IL-17F/CCL20 axis may be a novel pharmacological target for asthma.

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9

Chen, Sijia, Iris C. Blijdorp, Leonieke J. J. van Mens, Rowann Bowcutt, Talia E. Latuhihin, Marleen G. H. van de Sande, Stevan Shaw, Nataliya G. Yeremenko y Dominique L. P. Baeten. "Interleukin 17A and IL-17F Expression and Functional Responses in Rheumatoid Arthritis and Peripheral Spondyloarthritis". Journal of Rheumatology 47, n.º 11 (15 de enero de 2020): 1606–13. http://dx.doi.org/10.3899/jrheum.190571.

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Objective.Targeting the interleukin 17 (IL-17) axis is efficacious in psoriasis and spondyloarthritis (SpA), but not in rheumatoid arthritis (RA). We investigated potential differences in tissue expression and function of IL-17A and IL-17F in these conditions.Methods.mRNA expression of cytokines and their receptors was assessed by quantitative PCR in psoriasis skin samples, in SpA and RA synovial tissue (ST) samples and in fibroblast-like synoviocytes (FLS). Cytokines were measured in synovial fluid (SF) and FLS supernatants by ELISA. FLS were stimulated with IL-17A or IL-17F cytokines supplemented with tumor necrosis factor (TNF), or with pooled SF from patients with SpA or RA.Results.Levels of IL-17A (P = 0.031) and IL-17F (P = 0.017) mRNA were lower in psoriatic arthritis ST compared to paired psoriasis skin samples. The level of IL-17A mRNA was 2.7-fold lower than that of IL-17F in skin (P = 0.0078), but 17.3-fold higher in ST (P < 0.0001). In SF, the level of IL-17A protein was 37.4-fold higher than that of IL-17F [median 292.4 (IQR 81.4–464.2) vs median 7.8 (IQR 7.7–8.7) pg/mL; P < 0.0001]. IL-17A and IL-17F mRNA and protein levels did not differ in SpA compared to RA synovitis samples, and neither were the IL-17 receptors IL-17RA and IL-17RC, or the TNF receptors TNFR1 and TNR2, differentially expressed between SpA and RA ST, nor between SpA and RA FLS. SpA and RA FLS produced similar amounts of IL-6 and IL-8 protein upon stimulation with IL-17A or IL-17F cytokines, supplemented with 1 ng/ml TNF. Pooled SpA or RA SF samples similarly enhanced the inflammatory response to IL-17A and IL-17F simulation in FLS.Conclusion.The IL-17A/IL-17F expression ratio is higher in SpA synovitis compared to psoriasis skin. Expression of IL-17A and IL-17F, and the functional response to these cytokines, appear to be similar in SpA and RA synovitis.

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10

Zhou, Chunsheng, Felix E. Y. Aggor, Leticia A. Monin, Rachael A. Gordon, Tara N. Edwards, Daniel H. Kaplan, Mark J. Shlomchik, Sebastien Gingras y Sarah L. Gaffen. "A naturally-occurring mutation in IL-17F reveals a protective role for the IL-17AF heterodimer in oropharyngeal candidiasis (OPC)". Journal of Immunology 204, n.º 1_Supplement (1 de mayo de 2020): 227.2. http://dx.doi.org/10.4049/jimmunol.204.supp.227.2.

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Abstract IL-17A is the original member of the IL-17 family of cytokines. Among the IL-17 family, IL-17F shares the most homology with IL-17A at the amino acid level. IL-17A and IL-17F exist as homodimers and also form a heterodimer (IL-17AF). All of these cytokine dimers signal through the same IL-17RA:IL-17RC receptor complex, but the ligands exhibit different signaling strengths (IL-17A > IL-17AF > IL-17F). We previously showed that IL-17 signaling is critical for immunity against oropharyngeal candidiasis (OPC), an opportunistic infection of the oral mucosa caused by the commensal fungus C. albicans. Mice lacking IL-17RA, IL-17RC, or the adaptor ACT1 all have higher oral fungal burdens than wild type (WT) following oral infection with C. albicans. IL-17A deficient mice are also mildly susceptible to C. albicans oral infection, but blockade of IL-17F does not cause disease susceptibility. Furthermore, double blockade of IL-17A and IL-17F during OPC reveals a cooperative antifungal activity of IL-17A and IL-17F. However, the role of the IL-17AF heterodimer still remains poorly understood. Here, we took advantage of a dominant-negative mutation (IL-17F.S65L) that was previously identified in chronic mucocutaneous candidiasis disease (CMCD) patients. This mutation blocks the signals of IL-17F and IL-17AF but not IL-17A. Using CRISPR/Cas9 technology, we created mice with the analogous IL-17F S65L mutation. These IL-17FS65L/S65L mice showed a similar degree of susceptibility as IL-17A−/− mice though less than IL-17RA−/− mice upon C. albicans oral infection. This result suggests that IL-17AF contributes to protection against OPC.

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Más fuentes

Tesis sobre el tema "IL-17F"

1

Walliser, Isabelle [Verfasser] y Thomas [Akademischer Betreuer] Göbel. "Membrangebundenes IL-17A und IL-17F zur Herstellung spezifischer monoklonaler Antikörper für die intrazytoplasmatische Zytokinfärbung / Isabelle Walliser ; Betreuer: Thomas Göbel". München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2017. http://d-nb.info/1138566144/34.

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Hummel, Ira. "Analyse der IL-17F-Expression und des IL17F p.His161Arg-Polymorphismus bei chronisch entzündlichen Darmerkrankungen: Auswirkungen auf die Krankheitssuszeptibilität und den Phänotyp". Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-142348.

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Hummel, Ira [Verfasser] y Julia [Akademischer Betreuer] Seiderer-Nack. "Analyse der IL-17F-Expression und des IL17F p.His161Arg-Polymorphismus bei chronisch entzündlichen Darmerkrankungen: Auswirkungen auf die Krankheitssuszeptibilität und den Phänotyp / Ira Hummel. Betreuer: Julia Seiderer-Nack". München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2012. http://d-nb.info/1022318888/34.

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TSAI, YI-SHAN y 蔡依珊. "Distinct Pathogenic Roles of IL-17A and IL-17F in the Pathogenesis IgA Nephropathy". Thesis, 2017. http://ndltd.ncl.edu.tw/handle/15091668552461685388.

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Capítulos de libros sobre el tema "IL-17F"

1

Biggs, Catherine M. y Stuart E. Turvey. "Chronic Mucocutaneous Candidiasis, IL-17F Deficiency". En Encyclopedia of Medical Immunology, 164–67. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-8678-7_61.

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Biggs, Catherine M. y Stuart E. Turvey. "Chronic Mucocutaneous Candidiasis, IL-17F Deficiency". En Encyclopedia of Medical Immunology, 1–4. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-9209-2_61-1.

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Ishigame, Harumichi y Susumu Nakae. "The Roles of IL-17A and IL-17F in Infection and Inflammatory Disorders". En Cytokine Frontiers, 79–101. Tokyo: Springer Japan, 2013. http://dx.doi.org/10.1007/978-4-431-54442-5_3.

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4

Ishigame, Harumichi, Susumu Nakae y Yoichiro Iwakura. "The Roles of IL-17A and IL-17F in Mucosal Infection and Allergy". En TH17 Cells in Health and Disease, 269–97. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-9371-7_15.

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Evans Adunyah, Samuel, Richard Akomeah, Fareed K.N. Arthur, Roland S. Cooper y Joshua C.M. Williams. "IL-17 Biological Effects and Signaling Mechanisms in Human Leukemia U937 Cells". En 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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Actas de conferencias sobre el tema "IL-17F"

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Fujita, Junichi, Mio Kawaguchi, Fumio Kokubu, Satoshi Matsukura, Masashi Kurokawa, Kyouko Nozato, Ano Satoshi et al. "IL-33 Induces IL-17F In Bronchial Epithelial Cells". En American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1386.

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Cole, S. y A. Maroof. "P089 Mucosal-associated invariant T (MAIT)-cell-derived IL-17A and IL-17F production is IL-23-independent and biased towards IL-17F". En 39th European Workshop for Rheumatology Research, 28 February–2 March 2019, Lyon, France. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2019.78.

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Cole, Suzanne, Catherine Simpson, Remi Okoye, Meryn Griffiths, Dominique Baeten, Stevan Shaw y Ash Maroof. "OP0302 MUCOSAL-ASSOCIATED INVARIANT T (MAIT)-CELL-DERIVED IL-17A AND IL-17F PRODUCTION IS IL-23-INDEPENDENT AND BIASED TOWARDS IL-17F". En Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.1914.

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Vazquez-Tello, Alejandro, Jessica Nadigel, Bruce D. Mazer, David H. Eidelman y Qutayba Hamid. "Expression Of IL-17A And IL-17F Cytokines In B Lymphocytes". En American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5682.

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Maroof, A., R. Okoye, T. Smallie, D. Baeten, S. Archer, C. Simpson, M. Griffiths y S. Shaw. "THU0038 Bimekizumab dual inhibition of IL-17A and IL-17F provides evidence of IL-17F contribution to chronic inflammation in disease-relevant cells". En Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.4966.

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Fujita, J., M. Kawaguchi, F. Kokubu, T. Homma, S. Suzuki, S. Matsukura, Y. Morishima et al. "A Novel Cytokine, IL-17F Induces IL-11 in Bronchial Epithelial Cells." En American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2820.

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Ota, Kyoko, Mio Kawaguchi, Fumio Kokubu, Satoshi Matsukura, Satoshi Ano, Mio Kawaguchi, Junichi Fujita et al. "IL-17F Induces CCL20 Expression In Bronchial Epithelial Cells". En American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1394.

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Maroof, Ash, Dominique Baeten, Sophie Archer, Meryn Griffiths y Stevan Shaw. "02.13 Il-17f contributes to human chronic inflammation in synovial tissue: Preclinical evidence with dual il-17a and il-17f inhibition with bimekizumab in psoriatic arthritis". En 37th European Workshop for Rheumatology Research 2–4 March 2017 Athens, Greece. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2016-211050.13.

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Noack, M. y P. MIOSSEC. "P099 Comparison of IL-17A and IL-17F effects on different cell types". En 39th European Workshop for Rheumatology Research, 28 February–2 March 2019, Lyon, France. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2019.87.

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Fujita, Junichi, Mio Kawaguchi, F. Kokubu, Satoshi Matsukura, Hironori Masuko, Gen Ohara, Satoshi Ano et al. "Induction Of IL-11 And IGF-I By IL-17F In Bronchial Epithelial Cells". En American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1394.

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