Статті в журналах: "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, no. 1_Supplement (April 1, 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, no. 5 (April 14, 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, and Ahmed Al-Samadi. "Interleukin-17F Has Anti-Tumor Effects in Oral Tongue Cancer." Cancers 11, no. 5 (May 11, 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, and 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, and Goro Matsuzaki. "Role of IL-17 in chronic pulmonary mycobacterial infection. (MPF1P.775)." Journal of Immunology 192, no. 1_Supplement (May 1, 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, and 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, no. 5 (May 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, and Nobuyuki Hizawa. "IL-17F Induces CCL20 in Bronchial Epithelial Cells." Journal of Allergy 2011 (October 13, 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, and Dominique L. P. Baeten. "Interleukin 17A and IL-17F Expression and Functional Responses in Rheumatoid Arthritis and Peripheral Spondyloarthritis." Journal of Rheumatology 47, no. 11 (January 15, 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, and 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, no. 1_Supplement (May 1, 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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11

Chenuet, Pauline, Louis Fauconnier, Fahima Madouri, Tiffany Marchiol, Nathalie Rouxel, Aurélie Ledru, Pascal Mauny, et al. "Neutralization of either IL-17A or IL-17F is sufficient to inhibit house dust mite induced allergic asthma in mice." Clinical Science 131, no. 20 (October 13, 2017): 2533–48. http://dx.doi.org/10.1042/cs20171034.

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T helper (Th)17 immune response participates in allergic lung inflammation and asthma is reduced in the absence of interleukin (IL)-17 in mice. Since IL-17A and IL-17F are induced and bind the shared receptor IL-17RA, we asked whether both IL-17A and IL-17F contribute to house dust mite (HDM) induced asthma. We report that allergic lung inflammation is attenuated in absence of either IL-17A or IL-17F with reduced airway hyperreactivity, eosinophilic inflammation, goblet cell hyperplasia, cytokine and chemokine production as found in absence of IL-17RA. Furthermore, specific antibody neutralization of either IL-17A or IL-17F given during the sensitization phase attenuated allergic lung inflammation and airway hyperreactivity. In vitro activation by HDM of primary dendritic cells revealed a comparable induction of CXCL1 and IL-6 expression and the response to IL-17A and IL-17F relied on IL-17RA signaling via the adaptor protein act1 in fibroblasts. Therefore, HDM-induced allergic respiratory response depends on IL-17RA via act1 signaling and inactivation of either IL-17A or IL-17F is sufficient to attenuate allergic asthma in mice.

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12

von Vietinghoff, Sibylle, and Klaus Ley. "Interleukin 17A controls Interleukin 17F production to maintain precise regulation of blood neutrophil counts in mice (133.8)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 133.8. http://dx.doi.org/10.4049/jimmunol.182.supp.133.8.

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Abstract Granulocyte colony-stimulating factor (G-CSF), its receptor and interleukin-17 receptor A (IL-17RA) are all required to maintain baseline neutrophil counts in mice. Here, we tested whether IL-17F could compensate and maintain baseline neutrophil counts in the absence of IL-17A. Unlike the reduced neutrophil counts found in IL-17RA deficient mice, neutrophil counts were mildly increased in IL-17A deficient (Il17a-/-) animals. There was no evidence for infection or altered neutrophil function. Plasma G-CSF and IL-17F levels were elevated in Il17a-/- compared to wild-type mice. IL-17F was mainly produced in the spleen and mesenteric lymph nodes, but IL-23 was unaltered in Il17a-/- mice. Instead, Il17a-/- splenocytes differentiated with IL-6, TGF-β and IL-23 ex-vivo produced significantly more IL-17F in response to IL-23 than wild-type cells. Adding recombinant IL-17A to Il17a-/-splenocyte cultures reduced IL-17F mRNA and protein secretion. These effects were also observed in wild-type but not IL-17RA deficient cells. We conclude that IL-17A mediated suppression of IL-17F production and secretion is relevant to maintain the normal setpoint of blood neutrophil counts in vivo.

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13

Glatt, Sophie, Dominique Baeten, Terry Baker, Meryn Griffiths, Lucian Ionescu, Alastair D. G. Lawson, Ash Maroof, et al. "Dual IL-17A and IL-17F neutralisation by bimekizumab in psoriatic arthritis: evidence from preclinical experiments and a randomised placebo-controlled clinical trial that IL-17F contributes to human chronic tissue inflammation." Annals of the Rheumatic Diseases 77, no. 4 (December 23, 2017): 523–32. http://dx.doi.org/10.1136/annrheumdis-2017-212127.

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ObjectiveInterleukin (IL)-17A has emerged as pivotal in driving tissue pathology in immune-mediated inflammatory diseases. The role of IL-17F, sharing 50% sequence homology and overlapping biological function, remains less clear. We hypothesised that IL-17F, together with IL-17A, contributes to chronic tissue inflammation, and that dual neutralisation may lead to more profound suppression of inflammation than inhibition of IL-17A alone.MethodsPreclinical experiments assessed the role of IL-17A and IL-17F in tissue inflammation using disease-relevant human cells. A placebo-controlled proof-of-concept (PoC) clinical trial randomised patients with psoriatic arthritis (PsA) to bimekizumab (n=39) or placebo (n=14). Safety, pharmacokinetics and clinical efficacy of multiple doses (weeks 0, 3, 6 (240 mg/160 mg/160 mg; 80 mg/40 mg/40 mg; 160 mg/80 mg/80 mg and 560 mg/320 mg/320 mg)) of bimekizumab, a humanised monoclonal IgG1 antibody neutralising both IL-17A and IL-17F, were investigated.ResultsIL-17F induced qualitatively similar inflammatory responses to IL-17A in skin and joint cells. Neutralisation of IL-17A and IL-17F with bimekizumab more effectively suppressed in vitro cytokine responses and neutrophil chemotaxis than inhibition of IL-17A or IL-17F alone. The PoC trial met both prespecified efficacy success criteria and showed rapid, profound responses in both joint and skin (pooled top three doses vs placebo at week 8: American College of Rheumatology 20% response criteria 80.0% vs 16.7% (posterior probability >99%); Psoriasis Area and Severity Index 100% response criteria 86.7% vs 0%), sustained to week 20, without unexpected safety signals.ConclusionsThese data support IL-17F as a key driver of human chronic tissue inflammation and the rationale for dual neutralisation of IL-17A and IL-17F in PsA and related conditions.Trial registration numberNCT02141763; Results.

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14

Puel, Anne, Sophie Cypowyj, Jacinta Bustamante, Jill Wright, Luyan Liu, Hye Kyung Lim, Mélanie Migaud, et al. "Chronic mucocutaneous candidiasis in humans with inborn errors of interleukin-17 immunity (114.16)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 114.16. http://dx.doi.org/10.4049/jimmunol.186.supp.114.16.

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Abstract Chronic mucocutaneous candidiasis disease (CMCD) is characterized by recurrent or persistent infections of the skin, nails, oral and genital mucosae caused by Candida albicans and, to a lesser extent, Staphylococcus aureus, in patients with no other infectious or autoimmune manifestations. We report two genetic etiologies of CMCD: autosomal recessive deficiency in the cytokine receptor, interleukin-17 receptor A (IL-17RA), and autosomal dominant deficiency of the cytokine IL-17F. IL-17RA deficiency is complete, abolishing cellular responses to IL-17A and IL-17F homo- and heterodimers. By contrast, IL-17F deficiency is partial, with mutant IL-17F-containing homo- and heterodimers displaying impaired, but not abolished activity. These experiments of nature indicate that human IL-17A and IL-17F are essential for mucocutaneous immunity against C. albicans, but otherwise largely redundant.

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Iznardo, Helena, and Lluís Puig. "Dual inhibition of IL-17A and IL-17F in psoriatic disease." Therapeutic Advances in Chronic Disease 12 (January 2021): 204062232110378. http://dx.doi.org/10.1177/20406223211037846.

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Psoriasis and psoriatic arthritis are chronic immune-mediated disorders with involvement of interleukin (IL)-17 cytokines in their pathogenesis. IL-17A has been considered to be the most biologically active, but IL-17F is also over-expressed in skin and synovial tissues of patients with these diseases. Many therapeutic advances have been made in the past years, but some needs remain unmet. Dual inhibitor and bispecific antibodies simultaneously targeting IL-17A and IL-17F could provide better disease control. Herein we review current evidence on bimekizumab and sonelokimab. The antigen-binding site of bimekizumab neutralizes both IL-17A and IL-17F; phase I, II, and III studies have demonstrated its efficacy and safety in psoriasis and psoriatic arthritis. Sonelokimab is a trivalent nanobody targeting IL-17A and IL-17F; phase I and II studies with this molecule have yielded promising results in psoriasis.

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Gan, Yuzhou, Xiaozhen Zhao, Jing He, Xu Liu, Yun Li, Xiaolin Sun, and Zhanguo Li. "Increased Interleukin-17F is Associated with Elevated Autoantibody Levels and More Clinically Relevant Than Interleukin-17A in Primary Sjögren’s Syndrome." Journal of Immunology Research 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/4768408.

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Th17 related immune response is pathogenic in primary Sjögren’s syndrome (pSS). However, the role of IL-17F, one potent inflammatory member of IL-17 family cytokines in pSS, has not been specifically defined. We recruited one hundred and nine pSS patients and forty-two healthy controls and their serum levels of IL-17A and IL-17F were determined by multiplex cytokine assays. White blood cell, red blood cell, neutrophil, lymphocyte, IgM, IgG, C3, C4, RF, ANA, anti-SSA antibody, and anti-SSB antibody were measured by standard laboratory techniques. EULAR Sjögren’s syndrome disease activity index (ESSDAI) score was also evaluated accordingly. We found that IL-17F was significantly increased in pSS patients. Elevated levels of IL-17F were associated with increased IgG and IgM, higher titers of ANA and anti-SSA antibodies, and reduction of C3 and C4. Patients with higher disease activity also showed higher serum IL-17F levels. However, serum IL-17A was only increased in patients with longer disease duration and showed few correlation with clinical and laboratory features in pSS patients. In conclusion, IL-17F was correlated with increased autoantibody levels and disease activity in pSS and is more clinically relevant than IL-17A.

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17

Prosekova, Elena V., Alina I. Turyanskaya, Maxim S. Dolgopolov, Oksana L. Zhdanova, and Vitaly A. Sabynych. "Analysis of the genotypes and interleukins 17A, 17F blood levels in children with allergic bronchial asthma and allergic rhinitis." Russian Journal of Allergy 17, no. 2 (July 23, 2020): 61–68. http://dx.doi.org/10.36691/rja1360.

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Introduction. The study of genes that control the activity of cytokines is one of the important issues in revealing the pathogenetic mechanisms of allergic diseases. Aims. Determination of the frequency of occurrence of polymorphic gene markers genotypes and characterization of the interleukins 17A, 17F content in blood serum in children with bronchial asthma and allergic rhinitis. Materials and methods. A comprehensive survey of 110 children with allergic diseases of 311 years old and 60 healthy peers. The material for genetic analysis was DNA with the study of mutation points of IL-17A at position 197 (GA) and IL-17F 7488 (TC). The content of IL-17A, IL-17F interleukins was measured by enzymelinked assay. For the statistical analysis we used the Statistica 10, methods for comparing unrelated groups of genotypes distributions to expected values at HardyWeinberg equilibrium with 2. Results. The frequency of occurrence of genotypes in a group of healthy children was as follows: IL-17A (G197A) heterozygous GA (63,333%), homozygous GG (36,667%); IL-17F (T7488C) TT (36,667%), CT (63,333%), genotypes AA and CC werent determined. In children with allergic diseases, all genotypes were determined: IL-17A (G197A), GG (11,818%), AA (19,091%) and GA (69,091%), IL-17F (T7488C), TT (5,454%), CC (35,455%) and CT (59,091%) with the highest specific gravity of the GG genotype and TT. There were no significant differences in IL-17A, IL-17F levels in the blood serum depending on the genotype. Discussion. There were significant differences in the structure of the polymorphisms of the IL-17A, IL-17F genes, blood levels of IL-17A, IL-17F and the risk of the disease in allergic children and healthy peers. The frequency of allergic diseases in children with genotypes AA and TT is statistically higher, but with genotypes GG, CC is statistically lower than with other genotypes.

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Iyoda, Masayuki, Takanori Shibata, Mio Kawaguchi, Nobuyuki Hizawa, Toshimitsu Yamaoka, Fumio Kokubu та Tadao Akizawa. "IL-17A and IL-17F stimulate chemokines via MAPK pathways (ERK1/2 and p38 but not JNK) in mouse cultured mesangial cells: synergy with TNF-α and IL-1β". American Journal of Physiology-Renal Physiology 298, № 3 (березень 2010): F779—F787. http://dx.doi.org/10.1152/ajprenal.00198.2009.

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We investigated the role of IL-17 family members IL-17A and IL-17F in the induction of chemokines in mouse cultured mesangial cells (SV40 MES 13 cells). We evaluated the expression of the chemokines monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-2 (MIP-2) by ELISA and real-time RT-PCR (Q-PCR). Activation of MAPK was assessed by immunoblotting. IL-17RA and IL-17RC were inhibited by small interfering RNA (siRNA). We found that IL-17A or IL-17F stimulation of mesangial cells led to both a dose- and time-dependent increase in MCP-1 and MIP-2 release. This effect was dependent on mRNA transcription and protein translation. Both also enhanced TNF-α- and IL-1β-mediated MCP-1 and MIP-2 release in the cells. Additionally, we observed that IL-17A and IL-17F induced MAPK (p38 MAPK, ERK1/2, and JNK) activation and that pharmacological inhibitors of p38 MAPK (SB203580) and ERK1/2 (U0126), but not JNK (SP600125), blocked the IL-17A/IL-17F-mediated MCP-1 and MIP-2 release. Mesangial cells expressed IL-17RA and IL-17RC, and the IL-17A-mediated MCP-1 and MIP-2 release was significantly blocked by soluble IL-17RA. Furthermore, inhibition of either IL-17RA or IL-17RC expression via siRNA led to significant reduction of IL-17A/IL-17F-stimulated chemokine production. We conclude that IL-17A and IL-17F induce the production of chemokines MCP-1 and MIP-2 via MAPK pathways (p38 MAPK and ERK1/2), as well as mRNA transcription and protein translation and have synergistic effects with TNF-α and IL-1β in cultured mesangial cells.

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Shah, Mittal, Asher Maroof, Panos Gikas, Gayatri Mittal, Richard Keen, Dominique Baeten, Stevan Shaw, and Scott J. Roberts. "Dual neutralisation of IL-17F and IL-17A with bimekizumab blocks inflammation-driven osteogenic differentiation of human periosteal cells." RMD Open 6, no. 2 (July 2020): e001306. http://dx.doi.org/10.1136/rmdopen-2020-001306.

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ObjectivesInterleukin (IL)-17 signalling has been shown to be a key regulator of disease in ankylosing spondylitis (AS) with several IL-17 blockers currently clinically approved. Despite this, the role of IL-17 in bone pathology is poorly understood. This study aimed to investigate IL-17 signalling in the context of pathological bone formation.MethodsA biomimetic human periosteum-derived cell (hPDC) model of osteogenic differentiation was used in combination with recombinant IL-17 cytokines, T-cell supernatants or serum from patients with AS. IL-17A, IL-17F and bimekizumab monoclonal antibodies were used to block IL-17 cytokine action.ResultsRecombinant IL-17A and IL-17F are pro-osteogenic with respect to hPDC differentiation. T helper 17 or γδ-T cell supernatants also potently stimulated in vitro bone formation, which was blocked deeper by dual inhibition of IL-17A and IL-17F than by neutralisation of IL-17A or IL-17F individually. Osteogenic blockade may be due to an increase in expression of the Wnt antagonist DKK1. Interestingly, osteocommitment was also induced by serum obtained from patients with AS, which was also abrogated by dual neutralisation of IL-17A and IL-17F.ConclusionsThese data show for the first time that IL-17A and IL-17F enhance in vitro osteogenic differentiation and bone formation from hPDCs, inhibition of which may offer an attractive therapeutic strategy to prevent pathological bone formation.

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Wielińska, Joanna, Jerzy Świerkot, Katarzyna Kolossa, Bartosz Bugaj, Monika Chaszczewska-Markowska, Sławomir Jeka, and Katarzyna Bogunia-Kubik. "Polymorphisms within Genes Coding for IL-17A and F and Their Receptor as Clinical Hallmarks in Ankylosing Spondylitis." Mediators of Inflammation 2021 (October 27, 2021): 1–9. http://dx.doi.org/10.1155/2021/3125922.

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IL-17A and IL-17F together with their coreceptor (IL-17RA/RC) were reported to play a significant role in the pathogenesis of spondyloarthritis. The group of axial spondyloarthritis comprises ankylosing spondylitis (AS), a rheumatic disease characterized by chronic inflammation of the joints in the spine. This study is aimed at investigating IL-17A, IL-17F, IL-17RA, and IL-17RC polymorphisms as potential biomarkers of disease susceptibility, clinical parameters, and anti-TNF treatment outcome in a cohort of Polish ankylosing spondylitis patients. In total, 328 subjects, including 138 AS patients and 190 healthy volunteers, participated in the study. Genotyping of IL-17A rs2275913 (G/A), IL-17F rs763780 (A/G), IL-17RA rs4819554 (A/G), and IL-17RC rs708567 (G/A) was performed on real-time PCR instrument using LightSNiP assays. No significant differences were revealed in genotype and allele distribution between patients and controls despite the association of the IL-17RC rs708567 AA homozygosity with the earlier onset of the disease. Moreover, some relationships between IL-17F rs763780 and IL-17RA rs4819554 polymorphisms with clinical parameters related to the disease activity and anti-TNF treatment outcome were observed. IL-17F rs763780 G allele was found to be associated with high disease activity and BASDAI after 6 months and poor response to the treatment while higher VAS values were more common among IL-17RA rs4819554 G variant carriers. In conclusion, the IL-17F rs763780 polymorphism should be considered as a promising biomarker of disease activity and anti-TNF treatment outcome. The IL-17RA rs48419554 G allele may serve as a potential marker of disease severity in Polish AS patients.

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Sweet, Kristen, Qingxuan Song, Matthew J. Loza, Iain B. McInnes, Keying Ma, Karen Leander, Vani Lakshminarayanan, Carol Franks, Philip Cooper, and Stefan Siebert. "Guselkumab induces robust reduction in acute phase proteins and type 17 effector cytokines in active psoriatic arthritis: results from phase 3 trials." RMD Open 7, no. 2 (May 2021): e001679. http://dx.doi.org/10.1136/rmdopen-2021-001679.

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ObjectiveTo investigate serum protein expression in participants with psoriatic arthritis (PsA) and changes after guselkumab treatment.MethodsParticipants with PsA were treated with guselkumab or placebo in the DISCOVER-1 and DISCOVER-2 studies. Serum levels of acute phase reactants C reactive protein (CRP) and serum amyloid A (SAA) and inflammatory cytokines/chemokines were measured at weeks 0, 4 and 24 in 300 study participants and 34 healthy controls (HCs). The PSUMMIT studies measured serum interleukin (IL)-17A, IL-17F and CRP after ustekinumab treatment and levels with ustekinumab versus guselkumab treatment were compared.ResultsBaseline serum levels of CRP, SAA, IL-6, IL-17A and IL-17F were elevated in participants with active PsA vs HCs (p<0.05, geometric mean (GM) ≥40% higher). Baseline T-helper cell 17 (Th17) effector cytokines were significantly associated with baseline psoriasis but not joint disease activity. Compared with placebo, guselkumab treatment resulted in decreases in serum CRP, SAA, IL-6, IL-17A, IL-17F and IL-22 as early as week 4 and continued to decrease through week 24 (p<0.05, GM decrease from baseline ≥33%). At week 24, IL-17A and IL-17F levels were not significantly different from HCs, suggesting normalisation of peripheral IL-23/Th17 axis effector cytokines postguselkumab treatment. Reductions in IL-17A/IL-17F levels were greater in guselkumab-treated versus ustekinumab-treated participants, whereas effects on CRP levels were similar.ConclusionGuselkumab treatment reduced serum protein levels of acute phase and Th17 effector cytokines and achieved comparable levels to those in HCs. In participants with PsA, reductions of IL-17A and IL-17F were of greater magnitude after treatment with guselkumab than with ustekinumab.

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Liang, Spencer C., Xiang-Yang Tan, Deborah P. Luxenberg, Riyez Karim, Kyriaki Dunussi-Joannopoulos, Mary Collins, and Lynette A. Fouser. "Interleukin (IL)-22 and IL-17 are coexpressed by Th17 cells and cooperatively enhance expression of antimicrobial peptides." Journal of Experimental Medicine 203, no. 10 (September 18, 2006): 2271–79. http://dx.doi.org/10.1084/jem.20061308.

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Th17 cells are a distinct lineage of effector CD4+ T cells characterized by their production of interleukin (IL)-17. We demonstrate that Th17 cells also expressed IL-22, an IL-10 family member, at substantially higher amounts than T helper (Th)1 or Th2 cells. Similar to IL-17A, IL-22 expression was initiated by transforming growth factor β signaling in the context of IL-6 and other proinflammatory cytokines. The subsequent expansion of IL-22–producing cells was dependent on IL-23. We further demonstrate that IL-22 was coexpressed in vitro and in vivo with both IL-17A and IL-17F. To study a functional relationship among these cytokines, we examined the expression of antimicrobial peptides by primary keratinocytes treated with combinations of IL-22, IL-17A, and IL-17F. IL-22 in conjunction with IL-17A or IL-17F synergistically induced the expression of β-defensin 2 and S100A9 and additively enhanced the expression of S100A7 and S100A8. Collectively, we have identified IL-22 as a new cytokine expressed by Th17 cells that synergizes with IL-17A or IL-17F to regulate genes associated with skin innate immunity.

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Schifano, Matthew, Mark A. P. Konrad, Gangzhou Li, Soha Araji, Natalie Ruiz, and Peggy Just. "Correlating the phenotype of in vitro-polarized Th17 cells with expression of IL-17A and IL-17F (47.6)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 47.6. http://dx.doi.org/10.4049/jimmunol.182.supp.47.6.

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Abstract The T-helper 17 (Th17) lineage has surfaced as a topic of great interest in the fields of inflammation and autoimmunity. The secretion of interleukin (IL)-17A and IL-17F has implicated these cells in many autoimmune diseases including rheumatoid arthritis, Crohn's disease, asthma and multiple sclerosis. IL-17A and IL-17F have been shown to form both homodimers and heterodimeric complexes. Characterization of the expression of these Th17 effector molecules together with surface proteins such as CCR6, CD161 and RORγt will be useful for studying further the role of Th17 cells in human disease. In this study, in vitro-polarized Th17 cells were analyzed for surface expression, secretion or intracellular expression of Th17-related proteins. Using an ELISA with minimal cross-reactivity to IL-17A/A and IL-17F/F, IL-17A/F was found to be a major product of in vitro-polarized Th17 cells. Furthermore, IL-17A/A expression was less than or equal to IL-17A/F, while IL-17F/F expression was consistently lower than IL-17A/A or IL-17A/F.

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Elsissy, Maha, Ahmed Abdelhafez, Manal Elmasry, and Doaa Salah. "Interleukin-17 Gene Polymorphism Is Protective Against the Susceptibility to Adult Acute Myeloid Leukaemia in Egypt: A Case-Control Study." Open Access Macedonian Journal of Medical Sciences 7, no. 9 (May 15, 2019): 1425–29. http://dx.doi.org/10.3889/oamjms.2019.306.

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BACKGROUND: Th17 cells are blamed for being accused in the pathogenesis of acute myeloid leukaemia. Th17 cells are CD4+ cell subtype. They produce IL-17A and IL-17F. AIM: This study aims to trace the relation between IL-17A and IL-17F polymorphisms and AML incidence and to define the connection between IL-17 polymorphisms and its serum level. METHODS: A group of 100 acute myeloid leukaemia patients and 100 age and sex-matched healthy subjects (controls) were enrolled in the present work. Restriction fragment length polymorphism- polymerase chain reaction (PCR-RFLP) was done to detect IL-17A (rs2275913; G197A) and IL-17F (rs763780; A7488G). Serum IL-17 level was assessed by Enzyme-linked immunosorbent assay analysis (ELISA) in both patients and controls. RESULTS: IL-17F, IL-17A mutant genotypes and alleles showed no significant relation with acute myeloid leukaemia incidence. Also, ELISA results proved that serum IL-17 did not vary between acute myeloid leukaemia patients and healthy subjects. CONCLUSION: Interleukin-17 gene polymorphisms did not consider a risk for acute myeloid leukaemia.

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Chen, Rongchang, Qingling Zhang, Shuyu Chen, Haixiong Tang, Peikai Huang, Shushan Wei, Zhenyu Liang, Xin Chen, Ailin Tao, and Lihong Yao. "IL-17F, rather than IL-17A, underlies airway inflammation in a steroid-insensitive toluene diisocyanate-induced asthma model." European Respiratory Journal 53, no. 4 (January 17, 2019): 1801510. http://dx.doi.org/10.1183/13993003.01510-2018.

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Steroid insensitivity constitutes a major problem for asthma management. Toluene diisocyanate (TDI) is one of the leading allergens of asthma that induces both T-helper Th2 and Th17 responses, and is often associated with poor responsiveness to steroid treatment in the clinic.We sought to evaluate the effects of inhaled and systemic steroids on a TDI-induced asthma model and to find how interleukin (IL)-17A and IL-17F function in this model. BALB/c mice were exposed to TDI for generating an asthma model and were treated with inhaled fluticasone propionate, systemic prednisone, anti-IL-17A, anti-IL-17F, recombinant IL-17A or IL-17F.Both fluticasone propionate and prednisone showed no effects on TDI-induced airway hyperresponsiveness (AHR), bronchial neutrophilia and eosinophilia, and epithelial goblet cell metaplasia. TDI-induced Th2 and Th17 signatures were not suppressed by fluticasone propionate or prednisone. Treatment with anti-IL-17A after TDI exposure led to increased AHR, aggravated mucus production and airway eosinophil recruitment, accompanied by amplified Th2 responses, whereas anti-IL-17F ameliorated TDI-induced AHR and airway neutrophilia, with decreased Th17 responses. Recombinant IL-17A and IL-17F showed opposite effects to the monoclonal antibodies.IL-17A and IL-17F exert distinct biological effects during airway inflammation of a TDI-induced asthma model, which is unresponsive to both inhaled and systemic steroids.

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Soytürk, Hayriye, and Murat Yılmaz. "A comparison of IL-17 and IL-34 concentrations in the cerebrospinal fluid of patients with acute inflammatory demyelinating neuropathy and chronic inflammatory demyelinating polyneuropathy." Revista da Associação Médica Brasileira 66, no. 11 (November 2020): 1583–88. http://dx.doi.org/10.1590/1806-9282.66.11.1583.

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SUMMARY OBJECTIVE: The role of interleukins, such as IL-17 and IL-34, in the pathogenesis of autoimmune diseases has been established in the literature. In the current study, we aimed to identify the concentrations of IL-17 (IL-17A, IL-17F) and IL-34 in the cerebrospinal fluid (CSF) of patients with chronic inflammatory demyelinating polyneuropathy (CIDP) and acute inflammatory demyelinating neuropathy (AIDN). METHODS: We included in this study 8 patients with CIDP (none of them receiving immunomodulatory or immunosuppressant therapy), 7 patients with Guillain-Barre syndrome (GBS, AIDN), and 7 control subjects. The CIDP and AIDN diagnoses were made by clinical evaluation and electrophysiological investigations according to international criteria. CSF samples were obtained appropriately, and the levels of IL-17A, IL-17F, and IL-34 were measured by ELISA kits. RESULTS: The concentrations of IL-17A, IL-17F, and IL-34 were higher in those with CIDP and AIDN compared to the controls (p=0.005, p=0.01, and p=0.001, respectively). While IL-34 levels were significantly higher in AIDN patients than in CIDP patients (p=0.04), there were no significant differences between the AIDN and CIDP groups with regard to the levels of IL-17A and IL-17F (p=0.4 and p=0.2, respectively) CONCLUSION: Our results indicate that IL-17A, IL-17F, and IL-34 levels may have a role in CIDP and AIDN. Furthermore, the difference in the IL-34 levels of patients with AIDN and CIDP may indicate an important difference between the pathogenesis of these two sets of the disease.

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Krejsgaard, Thorbjørn, Ivan V. Litvinov, Yang Wang, Lixin Xia, Andreas Willerslev-Olsen, Sergei B. Koralov, Katharina L. Kopp, et al. "Elucidating the role of interleukin-17F in cutaneous T-cell lymphoma." Blood 122, no. 6 (August 8, 2013): 943–50. http://dx.doi.org/10.1182/blood-2013-01-480889.

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Azadegan-Dehkordi, Fatemeh, Ardeshir Abbasi, Amin Talebi Bezmin Abadi, Khaled Minooie, Parya Aslani, Razieh Sadat Hosseini, and Farid Zandi. "From genes polymorphisms to mucosal expression of cytokines: evaluating IL-23/IL-17 axis in adult patients with gastritis." African Health Sciences 20, no. 3 (October 7, 2020): 1452–62. http://dx.doi.org/10.4314/ahs.v20i3.51.

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Background and Objective: Chronic inflammation is the typical sign of gastritis that may shift into gastric cancer. IL- 17A and IL-17F as a novel inflammatory cytokines subset of CD4+Th play the main role in inflammation. A key cytokine receptor in the inflammatory IL-17/IL-23 axis, the interleukin 23 receptor (IL23R), may be related to gastritis. We evaluated the correspondence between IL-17A G197A, IL-17F A7488G and IL23R+2199 A/C polymorphisms with TGF-β1, IL-6, IL-17, IL-21 and IL-23 mucosal mRNAs expression in uninfected H. Pylori (HP) chronic gastritis patients. Materials and Methods: Total RNA and genomic DNA were separated from gastric biopsies of 44 patients with gastritis. Subsequently, mucosal mRNAs expression of TGF-β1, IL-6, IL-17, IL-21 and IL-23 were assessed by real-time PCR. To polymorphisms determination of IL-17A G197A, IL-17F A7488G and IL-23R +2199A/C the PCR-RFLP was used in gastric biopsies. Results: Results point that IL-17A G197A, IL-17F A7488G and IL23R +2199A/C polymorphisms did not influence the mucosal expression of TGF-β1, IL-6, IL-17 and IL-21 (p> 0.05). In an opposite result, we don’t find a correspondence between IL-17A G197A, IL-17F A7488G polymorphisms and mucosal expression of IL-23 (p> 0.05). In a contrary, we found a correlation between IL23R +2199A/C polymorphism and mucosal expression of IL-23 in patients with chronic gastritis (p< 0.05). Conclusion: These findings propose that IL23R +2199A/C polymorphism may change the mucosal expression of IL-23 pattern in patients with gastritis disease in the absence of HP, but to support the conclusion, more research may be required. Keywords: Cytokines; polymorphism; gastritis; IL-23, IL-17.

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Shen, Wei, Wenqing Li, Lionel Feigenbaum, Julie Hixon, and Scott Durum. "Differential expression of IL-17A and Il-17F in inflammatory bowel disease/colon cancer using a new IL-17A/F-dual-color reporter mouse (114.1)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 114.1. http://dx.doi.org/10.4049/jimmunol.186.supp.114.1.

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Abstract Interleukin (IL) 17A and IL-17F are products of Th17 cells which are associated with autoimmunity and many inflammatory diseases such as rheumatoid arthritis and inflammatory bowel disease. Some studies have suggested that production and activity of these two cytokines may be different and we sought to visualize them simultaneously in the inflamed bowel. A bacterial artificial chromosome was modified to introduce two fluorescent reporter genes, tdTomato and GFP, into the linked IL-17A and IL-17F genes respectively. Mice were generated that harbor the BAC construct. In vitro, splenic T cells cultured under Th17 conditions showed single expressing cells and dual expressing cells. In vivo colonic intraepithelial cells in DSS-induced acute mouse colitis showed slightly more IL-17A reporter than IL-17F, while in AOM/DSS induced chronic mouse colitis model, much more IL-17A reporter than IL-17F was expressed. In the T cell (CD4+CD45RBhigh) transfer colitis model, only expression of the IL-17A reporter could be detected in intestinal intraepithelial cells of Rag1-/- recipients. These IL-17A/F-dual-color reporter mice should prove useful in determining the sites of microenvironmental triggers of activation of Th17 cells and other cells that produce IL-17A and F.

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Hall, Aisling O’Hara, Jennifer E. Towne, and Scott E. Plevy. "Get the IL-17F outta here!" Nature Immunology 19, no. 7 (June 18, 2018): 648–50. http://dx.doi.org/10.1038/s41590-018-0141-z.

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Whibley, Natasha, Anna Mamo, Heather Conti, Elisabetta Traggiai, Frank Kolbinger, Beate Vogel, Michael Kammueller, Ulrich Siebenlist, Yoichiro Iwakura, and Sarah Gaffen. "Differential requirements of IL-17 family cytokines in host defense against oral candidiasis (CCR6P.272)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 182.4. http://dx.doi.org/10.4049/jimmunol.192.supp.182.4.

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Abstract Antibodies against IL-17A and IL-17RA are in clinical trials for autoimmunity. Mutations in IL-17 signaling genes (IL17RA, IL17F, ACT1) cause susceptibility to mucocutaneous infection by the fungus Candida albicans. IL-17A, IL-17F and IL-17C all signal via IL-17RA, but their individual roles in controlling candidiasis are poorly defined. Accordingly, in vivo Ab neutralization of cytokines or knockout mice were evaluated in a model of oropharyngeal candidiasis (OPC). Following C. albicans exposure, tongue fungal burden after 4 d, weight change and target gene expression were assessed. Anti-IL-17A-treated mice showed modestly impaired clearance compared to WT at d4, whereas α-IL-17F-treated mice were not affected. However, IL-17RA-/- and Act1-/- mice were far more susceptible to OPC than α-IL-17A treated mice at 4 and 14 d, indicating contributions to immunity beyond IL-17A. Susceptibility was associated with reduced expression of IL-17-regulated genes encoding chemokines and defensins. In contrast to α-IL-17A-treated mice, IL-17A-/- mice showed no significant susceptibility to OPC. This discrepancy was not explained by contributions from IL-17F or IL-17C, because α-IL-17F-treated IL-17A-/- mice and IL-17C-/- mice cleared the infection as well as WT mice. The increased susceptibility of IL-17RA-/- and Act1-/- mice vs. those lacking specific cytokines implies compensation between IL-17 family cytokines and possibly additional antifungal effectors. Funded by Novartis and NIDCR.

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Kisand, Kai, Anette S. Bøe Wolff, Katarina Trebušak Podkrajšek, Liina Tserel, Maire Link, Kalle V. Kisand, Elisabeth Ersvaer, et al. "Chronic mucocutaneous candidiasis in APECED or thymoma patients correlates with autoimmunity to Th17-associated cytokines." Journal of Experimental Medicine 207, no. 2 (February 1, 2010): 299–308. http://dx.doi.org/10.1084/jem.20091669.

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Chronic mucocutaneous candidiasis (CMC) is frequently associated with T cell immunodeficiencies. Specifically, the proinflammatory IL-17A–producing Th17 subset is implicated in protection against fungi at epithelial surfaces. In autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED, or autoimmune polyendocrine syndrome 1), CMC is often the first sign, but the underlying immunodeficiency is a long-standing puzzle. In contrast, the subsequent endocrine features are clearly autoimmune, resulting from defects in thymic self-tolerance induction caused by mutations in the autoimmune regulator (AIRE). We report severely reduced IL-17F and IL-22 responses to both Candida albicans antigens and polyclonal stimulation in APECED patients with CMC. Surprisingly, these reductions are strongly associated with neutralizing autoantibodies to IL-17F and IL-22, whereas responses were normal and autoantibodies infrequent in APECED patients without CMC. Our multicenter survey revealed neutralizing autoantibodies against IL-17A (41%), IL-17F (75%), and/ or IL-22 (91%) in >150 APECED patients, especially those with CMC. We independently found autoantibodies against these Th17-produced cytokines in rare thymoma patients with CMC. The autoantibodies preceded the CMC in all informative cases. We conclude that IL-22 and IL-17F are key natural defenders against CMC and that the immunodeficiency underlying CMC in both patient groups has an autoimmune basis.

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Lee, Youngae, Yutaro Kumagai, Min Seong Jang, Jung-Hwan Kim, Bo-Gie Yang, Shizuo Akira та Myoung Ho Jang. "Intestinal Lin-c-Kit+NKp46-CD4- population highly produces IL-22 upon IL-1β stimulation (P3260)". Journal of Immunology 190, № 1_Supplement (1 травня 2013): 136.12. http://dx.doi.org/10.4049/jimmunol.190.supp.136.12.

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Abstract Small intestinal innate lymphoid cells (ILCs) regulate intestinal epithelial cell homeostasis and prevent pathogenic bacterial infections by producing IL-22. NKp46+ ILC (ILC22) and CD4+ ILC (CD4+ LTi) are known as main sources for IL-22 in the small intestine. We found that Lin-c-Kit+NKp46-CD4- (CD4- LTi), ILC22, and CD4+ LTi cells comprised 0.30 ± 0.03%, 1.10 ± 0.12%, and 0.07 ± 0.01%, respectively, of the total lymphocytes in the small intestinal lamina propria of adult mice (BALB/c). We next compared the induction of IL-17F and IL-22 among CD4- LTi, ILC22, and CD4+ LTi cells under stimulation with IL-1β or IL-23 or IL-1β and IL-23 stimulation, by real-time PCR, Bio-Plex analysis, and intracellular staining. We found here that CD4- LTi cells that expressed RORγt and IL-7Rα strongly expressed the transcripts for Il17f and Il22, and produced the proteins for IL-17F and IL-22 after stimulation with IL-1β and IL-23 stimulation compared with ILC22 and CD4+ LTi cells. However, none of CD4- LTi, ILC22, and CD4+ LTi cells produced IL-17F and IL-22 after stimulation with Pam3CSK4 (TLR2 ligand), Poly(I:C) (TLR3 ligand), or LPS (TLR4 ligand) for 24 hrs. Taken together, these findings indicate that the Lin-c-Kit+NKp46-CD4- population may control intestinal homeostasis and provide intestinal protection by producing high levels of IL-17F and IL-22 under the stimulation with IL-1β and IL-23.

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Vazquez-Tello, Alejandro, Rabih Halwani, Rui Li, Jessica Nadigel, Amir Bar-Or, Bruce D. Mazer, David H. Eidelman, Saleh Al-Muhsen, and Qutayba Hamid. "IL-17A and IL-17F Expression in B Lymphocytes." International Archives of Allergy and Immunology 157, no. 4 (November 25, 2011): 406–16. http://dx.doi.org/10.1159/000329527.

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Tan, Weihong, Weitao Huang, Xiaogang Gu, Qiu Zhong, Bainan Liu, and Paul Schwarzenberger. "IL-17F/IL-17R interaction stimulates granulopoiesis in mice." Experimental Hematology 36, no. 11 (November 2008): 1417–27. http://dx.doi.org/10.1016/j.exphem.2008.06.003.

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36

Algood, Holly Marie Scott, Beverly R. E. A. Dixon, Tiffany J. Lee, and M. Blanca Piazuelo. "IL-17A or IL-17F is sufficient to maintain innate response and control of H. pylori immunopathogenesis." Journal of Immunology 206, no. 1_Supplement (May 1, 2021): 99.28. http://dx.doi.org/10.4049/jimmunol.206.supp.99.28.

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Abstract Interleukin-17 receptor (IL-17R) signaling is required for control of many extracellular pathogens due to its impact on neutrophil recruitment and antimicrobial responses. Infection with the extracellular pathogen Helicobacter pylori results in Th1 and Th17 cell activation and a chronic inflammatory process which can lead to adverse outcomes such as gastric cancer. Previously, we identified IL-17RA as a requirement for the recruitment of neutrophils. Surprisingly, H. pylori infected IL-17RA−/− mice had significantly more chronic inflammation than H. pylori infected WT mice. In the current study, in vitro human epithelial cell cultures and in vivo mouse models were used to investigate differential roles for IL-17A, IL-17F and IL-17A/F during H. pylori infection. The data indicate generally that epithelial cells responded to IL-17A or IL-17A/F better than IL-17F. Increased gene expression of some factors, such as Cxcl8, required a co-stimulus such as H. pylori, TNF or IL-22 in epithelial cells, but expression of Pigr and Nox1 were induced by IL-17A alone. In vivo deficiencies of IL-17A or IL-17F alone did not significantly change the immunopathological response to H. pylori, but if both cytokines were absent, a hyperinflammatory lymphocytic response developed similar to what was observed in IL-17RA−/− mice. These data imply that IL-17A and IL-17F may have some overlapping role or compensatory roles in maintenance of the gastric mucosal response to infection which is required for preventing immunopathology.

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Atta, R. Z., and R. M. Aloubaidy. "GENETIC POLYMORPHISM OF ASTHMA IN IRAQ." IRAQI JOURNAL OF AGRICULTURAL SCIENCES 53, no. 2 (April 29, 2022): 288–96. http://dx.doi.org/10.36103/ijas.v53i2.1536.

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This case-control study was conducted to evaluate the influence of interleukin (IL) - 17A and -17F gene polymorphisms on the risk of asthma. In the present study blood samples were collected from 45 asthma patients and 50 healthy controls. Serum levels of cytokines interleukin-17A and interlukin-17F (IL-17A and IL17F, respectively) and immunoglobulin E (IgE) were measured using ELISA kit in both subjects. Serum levels of IL-17A and IgE were shown a higher significant differences (p< 0.05) while no significance difference ( p>0.05 )of IL-17F was shown in serum levels in comparison with controls . The frequency of the allele and genotypes in the patient groups and control groups were determined using Polymerase Chain Reaction Restriction Fragment Length Polymorphism (PCR-RFLP). IL-17A gene amplified using specific primers then digested by (XagI) restriction enzyme, in order to detect (G197A) (rs2275913) SNP. While IL-17F gene amplified using specific primers then digested with (Nla III) restriction enzyme to detect (A7488G) (rs763780) SNP. There were no significant differences between asthma patients and wild type GG and G allele and mutant type AA and A allele for IL-17A SNP (GG: OR 1.71, P=0.284, G: OR 1.71, P=1.00, AA: OR 1.99, P =0.294, A: OR 0.96, P=1.00) while the mutant type AG for mentioned SNP was determined and tested for their association significantly with asthmatic patients (OR 0.39, P=0.039). Frequencies of IL-17F genotype AA and allele A and mutant type AG or GG were found no associated with asthma patients.

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Banuelos, Jesus, Soon Shin, and Nick Lu. "Distinct glucocorticoid sensitivity of Th17 cytokines in murine T hybridomas and primary cells (IRC11P.428)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 197.10. http://dx.doi.org/10.4049/jimmunol.194.supp.197.10.

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Abstract Cytokine suppression contributes to the anti-inflammatory actions of glucocorticoids (GCs). However, IL-17 has been reported to be resistant to GC regulation in asthma, nasal polyps, and Crohn’s disease. In contrast, a negative GC-response element has been identified in the promoter region of the IL-17 gene and IL-17 was sensitive to GC suppression in a murine asthma model. To clarify whether IL-17 and other Th17 cytokines are sensitive to GC regulation, we generated Th17 hybridoma cells by fusing in vitro differentiated murine (bl/6) Th17 cells with BW5147 thymoma. Two clones selectively expressing IL-17A, IL-17F, IL-22 and GM-CSF were stable for over 30 generations. Additional clones selectively expressing IFN-γ or IL-4, but not Th17 cytokines and BW5147 cells that produce little or no cytokines were used as controls. Dexamethasone, a potent GC, significantly inhibited anti-CD3 and anti-CD28-stimulated IFN-γ, IL-4, as well as IL-17A, IL-17F, and IL-22 in various clones. Interestingly, IL-17A and IL-17F, but not IL-22, were resistant to GC suppression in in vitro differentiated Th17 cells. Furthermore, hybridomas, but not in vitro differentiated Th17 cells underwent GC-induced apoptosis. IL-6 partially rescues hybridomas from GC-induced apoptosis, however it did not modulate IL-17 suppression by GCs. Our findings support that IL-17A and IL-17F are capable of being downregulated by GCs and Th17 cell microenvironment and cellular milleu engender GC resistance.

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Schifano, Matthew, Soha Araji, Shourong Li, Natalie Ruiz, Nicolas Schrantz, Qiulong Huang, and Peggy Just. "A novel monoclonal antibody against the human IL-17AF heterodimer for flow cytometry (59.11)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 59.11. http://dx.doi.org/10.4049/jimmunol.188.supp.59.11.

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Abstract The IL-17 family members, IL-17A and IL-17F, are signature Th17 cytokines. Although they were both originally found to be produced as disulfide-linked homodimers, recent studies have confirmed the production of IL-17AF heterodimers in in vitro-differentiated and polarized Th17 cells. While ELISA-based assays have become available for the study of these heterodimers, flow antibodies have been generated only to the monomeric subunits, making discrimination between the homo- and heterodimer complexes difficult. Here, for the first time, we use a novel monoclonal antibody to identify producers of the IL-17AF heterodimer by flow cytometry. Under our polarization conditions, the majority of human lymphocytes that stain for both IL-17A and IL-17F also stain for the IL-17AF heterodimer. These results suggest that this population produces mostly IL-17AF heterodimers and not the IL-17A and IL-17F homodimers alone. This novel reagent will help expand our knowledge of the IL-17/Th17 axis and contribute to the elucidation of its role in the immune response.

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40

Губина, М. А., И. Г. Соловьева, В. Н. Бабенко, М. М. Черенкова, and А. Ю. Губина. "The study of gene polymorphisms of the IL-17 family in patients with gastric cancer of the West Siberian region." Nauchno-prakticheskii zhurnal «Medicinskaia genetika», no. 6(215) (June 29, 2020): 73–74. http://dx.doi.org/10.25557/2073-7998.2020.06.73-74.

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Проведен анализ IL-17A G197A и IL-17FA7488G у 150 человек, больных раком желудка, и 103 здоровых. Изученные группы сопоставимы по полу и возрасту. В контроле распределение генотипа для каждого SNP находится в равновесии Харди - Вайнберга. (р> 0,05). Частоты генотипов IL-17F A7488G у больных (GG 38,7%; GA 39,3% и AA 22%) значительно отличались от таковых в контроле (GG 16,5%; GA 60,2% и AA 23,3%). Генотипы IL-17A197 у больных также отличались от таковых в контроле (АА 40,7%; AG 48,7%; GG 10,6%; АА 17,5%; AG 70,8%; GG, 11.7%, соответственно). Полученные нами данные возможно свидетельствуют, что генотипы GG IL-17F A7488G и АА IL-17A197 связаны с риском развития рака желудка. The analysis of IL-17A G197A and IL-17FA7488G in 150 patients with gastric cancer and 103 healthy. The studied groups are comparable by gender and age. Among the controls, the genotype distribution for each SNP is in Hardy-Weinberg equilibrium. (p> 0.05). The frequencies of IL-17F A7488G genotypes in cases (GG - 38.7%; GA - 39.3% and AA, 22%) significantly differed from those in the control (GG, 16.5%; GA, 60.2% and AA, 23.3%). The genotypes of IL-17A197 in cases also differed from those in the control (AA 40.7%; AG, 48.7%; GG, 10.6% and AA 17.5%; AG, 70.8%; GG, 11.7%, respectively). Our data may indicate that the genotypes GG, IL-17F A7488G and AA, IL-17A197 are associated with a risk of developing gastric cancer.

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Sorbello, V., G. Ciprandi, A. Di Stefano, G. M. Massaglia, G. Favatà, S. Conticello, M. Malerba, et al. "Nasal IL-17F is related to bronchial IL-17F/neutrophilia and exacerbations in stable atopic severe asthma." Allergy 70, no. 2 (January 13, 2015): 236–40. http://dx.doi.org/10.1111/all.12547.

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42

Puel, Anne, Rainer Döffinger, Angels Natividad, Maya Chrabieh, Gabriela Barcenas-Morales, Capucine Picard, Aurélie Cobat, et al. "Autoantibodies against IL-17A, IL-17F, and IL-22 in patients with chronic mucocutaneous candidiasis and autoimmune polyendocrine syndrome type I." Journal of Experimental Medicine 207, no. 2 (February 1, 2010): 291–97. http://dx.doi.org/10.1084/jem.20091983.

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Most patients with autoimmune polyendocrine syndrome type I (APS-I) display chronic mucocutaneous candidiasis (CMC). We hypothesized that this CMC might result from autoimmunity to interleukin (IL)-17 cytokines. We found high titers of autoantibodies (auto-Abs) against IL-17A, IL-17F, and/or IL-22 in the sera of all 33 patients tested, as detected by multiplex particle-based flow cytometry. The auto-Abs against IL-17A, IL-17F, and IL-22 were specific in the five patients tested, as shown by Western blotting. The auto-Abs against IL-17A were neutralizing in the only patient tested, as shown by bioassays of IL-17A activity. None of the 37 healthy controls and none of the 103 patients with other autoimmune disorders tested had such auto-Abs. None of the patients with APS-I had auto-Abs against cytokines previously shown to cause other well-defined clinical syndromes in other patients (IL-6, interferon [IFN]-γ, or granulocyte/macrophage colony-stimulating factor) or against other cytokines (IL-1β, IL-10, IL-12, IL-18, IL-21, IL-23, IL-26, IFN-β, tumor necrosis factor [α], or transforming growth factor β). These findings suggest that auto-Abs against IL-17A, IL-17F, and IL-22 may cause CMC in patients with APS-I.

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Cole, S., C. Simpson, R. Okoye, M. Griffiths, D. Baeten, S. Shaw, and A. Maroof. "064 Mucosal-associated invariant T (MAIT) cell-derived IL-17A and IL-17F production is IL-23-independent and biased towards IL-17F." Journal of Investigative Dermatology 139, no. 5 (May 2019): S11. http://dx.doi.org/10.1016/j.jid.2019.03.140.

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Yu, Yiyun, Sisi Fu, Xianglin Zhang, Lingbiao Wang, Li Zhao, Weiguo Wan, Yu Xue, and Ling Lv. "Leptin facilitates the differentiation of Th17 cells from MRL/Mp-Fas lpr lupus mice by activating NLRP3 inflammasome." Innate Immunity 26, no. 4 (November 21, 2019): 294–300. http://dx.doi.org/10.1177/1753425919886643.

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Both NLRP3 inflammasome and Th17 cells play important roles in the pathogenesis of systemic lupus erythematosus (SLE). Here we tried to investigate whether leptin promotes the differentiation of Th17 cells from lupus mice by activating the NLRP3 inflammasome. Th17 cells induced from MRL/Mp-Fas lpr mice splenocytes under Th17 polarizing condition were treated with leptin at scalar doses during the last 18 h of culture. The mRNA levels of IL-17A, IL-17F, RORγt, IL-1β, IL-18, NLRP3, ASC, and IL-1R1 were detected by quantitative PCR. IL-17A, IL-17F, IL-1β, and IL-18 were tested by ELISA, while the activity of caspase-1 and number of Th17 cells were counted by flow cytometry before/after inhibition of the NLRP3 inflammasome. We found that leptin pushed up the expression of IL-17A, IL-17F, NLRP3, and IL-1β and increased the number of Th17 cells in lupus mice, while the expression of IL-17A, RORγt, and IL-1β and the number of Th17 cells were decreased after inhibition of the NLRP3 inflammasome. Leptin promoted the differentiation of Th17 cells from lupus mice by activating the NLRP3 inflammasome.

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El-Desoky, Manal M., Samar Tharwat, Nora Mostafa, Asem A. Hewidy, Rehab A. Elmorsey, Mona S. Abdelhafez, Amira H. El-Ashry, Mona M. Elhendawi, Aya Ahmed Fathy, and Fatma Azzahraa Hisham. "Association of Interleukin-17F Polymorphism and Mortality Predictors with the Risk of COVID-19." International Journal of Clinical Practice 2022 (October 27, 2022): 1–8. http://dx.doi.org/10.1155/2022/4761631.

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Background. Th-17 cells, a proinflammatory subset of CD4 T lymphocytes, have been suggested as a possible cause of coronavirus disease-19 (COVID-19)-related immunological injuries. The aim of this study was to investigate the relationship between IL-17F (rs763780) polymorphism and the susceptibility to and outcomes of COVID-19 infection and to determine the clinical and laboratory predictors of COVID-19 death. Methods. This case-control study included 132 COVID-19 patients and 135 healthy age- and sex-matched controls. The participants were tested for IL-17F rs763780 polymorphism via TaqMan-based genotyping and for the expression of IL-17 by enzyme-linked immunosorbent assay. This study also investigated the predictors for COVID-19 mortality. Results. A non-statistically significant association was observed between IL-17F alleles and genotypes with COVID-19 ( P = 0.309 , P = 0.138 , respectively). Moreover, no significant difference in the IL-17F genotypes was observed between non-survivors and survivors ( P = 0.482 ). In the multivariate analysis, the participants with the following characteristics had 17.7-, 11.2-, 8-, and 17.9-fold higher odds of exhibiting in-hospital mortality, respectively: (1) hypertension, (2) age of >57 years, (3) WBC count of >12.6 × 103/mm3, and (4) D-dimer of >0.9 ng/ml. The ROC curve analysis showed that IL-17 at a cutoff point of >46 pg/ml was a perfect discriminator of COVID-19 patients from control subjects (AUC = 1.0). Conclusion. The findings indicate that the IL-17F H161R variant does not influence the risk of COVID-19. However, the IL-17 level is a perfect discriminator of COVID-19 infection. Hypertension, age of >57 years, white blood cell count of >12.6 × 103/mm3, and D-dimer of >0.9 ng/ml are the independent predictors for death among COVID-19 patients.

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Bastidas-Coral, Angela P., Astrid D. Bakker, Behrouz Zandieh-Doulabi, Cornelis J. Kleverlaan, Nathalie Bravenboer, Tim Forouzanfar та Jenneke Klein-Nulend. "Cytokines TNF-α, IL-6, IL-17F, and IL-4 Differentially Affect Osteogenic Differentiation of Human Adipose Stem Cells". Stem Cells International 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/1318256.

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During the initial stages of bone repair, proinflammatory cytokines are released within the injury site, quickly followed by a shift to anti-inflammatory cytokines. The effect of pro- and anti-inflammatory cytokines on osteogenic differentiation of mesenchymal stem cells is controversial. Here, we investigated the effect of the proinflammatory cytokines TNF-α, IL-6, IL-8, and IL-17F and the anti-inflammatory cytokine IL-4 on proliferation and osteogenic differentiation of human adipose stem cells (hASCs). hASCs were treated with TNF-α, IL-6, IL-8, IL-17F, or IL-4 (10 ng/mL) for 72 h mimicking bone repair. TNF-αreduced collagen type I gene expression but increased hASC proliferation and ALP activity. IL-6 also strongly enhanced ALP activity (18-fold), as well as bone nodule formation by hASCs. IL-8 did not affect proliferation or osteogenic gene expression but reduced bone nodule formation. IL-17F decreased hASC proliferation but enhanced ALP activity. IL-4 enhanced osteocalcin gene expression and ALP activity but reduced RUNX2 gene expression and bone nodule formation. In conclusion, all cytokines studied have both enhancing and reducing effects on osteogenic differentiation of hASCs, even when applied for 72 h only. Some cytokines, specifically IL-6, may be suitable to induce osteogenic differentiation of mesenchymal stem cells as a strategy for enhancing bone repair.

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Kowerda, Anna Parfieniuk, Magdalena Swidersk, Tomasz Szulzyk, Jerzy Jaroszewicz, Tadeusz W. Lapinski, and Robert Flisiak. "Serum Concentrations of Th17-Associated Interleukins and Autoimmune Phenomena are Associated with the Degree of Liver Damage in Alcoholic Liver Disease." Journal of Gastrointestinal and Liver Diseases 26, no. 3 (September 1, 2017): 269–74. http://dx.doi.org/10.15403/jgld.2014.1121.263.pak.

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Background & Aims: Recent reports suggest an involvement of Th17 responses in inflammatory and autoimmune reactions in alcoholic liver disease (ALD). Our study aimed to assess serum levels of Th17-interleukins in ALD with regard to the frequency of liver-specific autoantibodies and degree of liver damage.Methods: Ninety-five patients with ALD were enrolled. Serum concentrations of IL-17F, IL-17A, IL-22 were assessed by ELISA. The presence of autoantibodies AMA-M2, SLA/LP, LKM-1, LC1, anti-F-actin, anti-desmin and anti-myosin in serum was assessed by immunoblotting, ANA antibodies were detected by ELISA. The results were analysed with regard to the degree of hepatic damage.Results: Serum IL-17F was significantly elevated in ALD patients compared to controls (p=0.03). There was a correlation between serum IL-17F and degree of liver failure evaluated by the MELD score (rs=0.23, p=0.03). Serum IL-22 also correlated with MELD score (rs=0.32, p=0.007) and CTP score (rs=0.28, p=0.02). Anti-F-actin antibodies were present in 19% and ANA-antibodies in 11% of the patients in the study group, and in no subjects in the control group. The prevalence of anti-F-actin autoantibodies was higher in subjects with more advanced liver diseases but also independently associated with IL-17A in the regression analysis. Furthermore, serum IL-22 in anti-F-actin(+)-patients was significantly higher compared to anti-F-actin(-)-patients (p=0.03).Conclusions: Elevation of serum IL-17A, IL-17F, IL-22 correlated with the progression of liver damage and also with presence of F-actin in ALD. Alcoholic liver disease may trigger autoimmunity and formation of autoantibodies, especially anti-F-actin, with possible engagement of Th17-related cytokines in this process.Abbreviations: AA: acetaldehyde; Abs: antibodies; AFP: α-fetoprotein; ALD: alcoholic liver disease; ALT: alanine aminotransferase; AMA-M2: antimitochondrial antibodies; ANA: antinuclear antibodies; ASMA: anti-smooth muscle antibodies; α-SMA: alpha smooth muscle actin; CTP Score: Child-Turcotte-Pugh Score; GAHS: Glasgow Alcoholic Hepatitis Score; GGT: γ-glutamyl transpeptidase; HBV: hepatitis B virus; HCV: hepatitis C virus; HIV: human immunodeficiency virus; HSCs: hepatic stellate cells; IL-β1: interleukin β1; IL-6: interleukin 6; IL-17A: interleukin 17A; IL-17F: interleukin 17F; IL-22: interleukin 22; KCs: Kupffer cells; LC1: liver cytosol antigen type 1; LKM-1: liver kidney microsomal antigen; MA: malondialdehyde; MELD: Model of End-Stage Liver Disease; NASH: non-alcoholic steatoheptatitis; SLA/LP: soluble liver antigen/liver-pancreas; TGF-β: tumour growth factor β; TNF-α: tumour necrosis factor α.

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48

Regen, Tommy, Sandrine Isaac, Ana Amorim, Nicolás Gonzalo Núñez, Judith Hauptmann, Arthi Shanmugavadivu, Matthias Klein, et al. "IL-17 controls central nervous system autoimmunity through the intestinal microbiome." Science Immunology 6, no. 56 (February 5, 2021): eaaz6563. http://dx.doi.org/10.1126/sciimmunol.aaz6563.

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Interleukin-17A– (IL-17A) and IL-17F–producing CD4+ T helper cells (TH17 cells) are implicated in the development of chronic inflammatory diseases, such as multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). TH17 cells also orchestrate leukocyte invasion of the central nervous system (CNS) and subsequent tissue damage. However, the role of IL-17A and IL-17F as effector cytokines is still confused with the encephalitogenic function of the cells that produce these cytokines, namely, TH17 cells, fueling a long-standing debate in the neuroimmunology field. Here, we demonstrated that mice deficient for IL-17A/F lose their susceptibility to EAE, which correlated with an altered composition of their gut microbiota. However, loss of IL-17A/F in TH cells did not diminish their encephalitogenic capacity. Reconstitution of a wild-type–like intestinal microbiota or reintroduction of IL-17A specifically into the gut epithelium of IL-17A/F–deficient mice reestablished their susceptibility to EAE. Thus, our data demonstrated that IL-17A and IL-17F are not encephalitogenic mediators but rather modulators of intestinal homeostasis that indirectly alter CNS-directed autoimmunity.

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Meeks, Karen D., Amy N. Sieve, Jay K. Kolls, and Rance E. Berg. "Interleukin-23 is required for protection against Listeria monocytogenes (133.24)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 133.24. http://dx.doi.org/10.4049/jimmunol.182.supp.133.24.

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Abstract Listeria monocytogenes (LM) is a gram-positive, intracellular bacterium that can induce spontaneous abortion, septicemia, and meningitis. Recently, it has been demonstrated that interleukin (IL)-17A is necessary for an optimal immune response against LM in the liver. As IL-23-dependent cytokines, IL-17A and IL-17F induce the mobilization of neutrophils to sites of infection. The importance of IL-23 during infection with LM has not been studied. We demonstrate here that IL-23 and the IL-17 receptor A (IL-17RA), which mediates both IL-17A and IL-17F signaling, are necessary for resistance against LM infection. During infection with LM, mice deficient in either IL-23 (IL-23p19 KO) or the IL-17RA (IL-17RA KO) have increased susceptibility to infection and increased bacterial burden in the spleen and liver. Interestingly, IL-17A, IL-17F, and IL-22 are decreased in supernatants from cells of LM infected IL-23p19 KO mice. Furthermore, neutrophils are decreased in IL-23p19 KO and IL-17RA KO mice at early time points. When IL-23p19 KO mice are rescued with the administration of exogenous IL-17A, a protective phenotype similar to that seen during infection of wild-type mice is achieved. Therefore, it is likely that IL-23 regulates the optimal production of IL-17A/F during LM infection which results in early neutrophil recruitment and bacterial clearance.

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KAWAGUCHI, M., D. TAKAHASHI, N. HIZAWA, S. SUZUKI, S. MATSUKURA, F. KOKUBU, Y. MAEDA, Y. FUKUI, S. KONNO, and S. HUANG. "IL-17F sequence variant (His161Arg) is associated with protection against asthma and antagonizes wild-type IL-17F activity." Journal of Allergy and Clinical Immunology 117, no. 4 (April 2006): 795–801. http://dx.doi.org/10.1016/j.jaci.2005.12.1346.

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