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https://www.readbyqxmd.com/read/29434599/rna-seq-analysis-of-il-1b-and-il-36-responses-in-epidermal-keratinocytes-identifies-a-shared-myd88-dependent-gene-signature
#1
William R Swindell, Maria A Beamer, Mrinal K Sarkar, Shannon Loftus, Joseph Fullmer, Xianying Xing, Nicole L Ward, Lam C Tsoi, Michelle J Kahlenberg, Yun Liang, Johann E Gudjonsson
IL-36 cytokines have recently emerged as mediators of inflammation in autoimmune conditions including psoriasis vulgaris (PsV) and generalized pustular psoriasis (GPP). This study used RNA-seq to profile the transcriptome of primary epidermal keratinocytes (KCs) treated with IL-1B, IL-36A, IL-36B, or IL-36G. We identified some early IL-1B-specific responses (8 h posttreatment), but nearly all late IL-1B responses were replicated by IL-36 cytokines (24 h posttreatment). Type I and II interferon genes exhibited time-dependent response patterns, with early induction (8 h) followed by no response or repression (24 h)...
2018: Frontiers in Immunology
https://www.readbyqxmd.com/read/29422292/autoinflammatory-keratinization-diseases-an-emerging-concept-encompassing-various-inflammatory-keratinization-disorders-of-the-skin
#2
Masashi Akiyama, Takuya Takeichi, John A McGrath, Kazumitsu Sugiura
Classifying inflammatory skin diseases is challenging, especially for the expanding group of disorders triggered by genetic factors resulting in hyperactivated innate immunity that result in overlapping patterns of dermal and epidermal inflammation with hyperkeratosis. For such conditions, the umbrella term "autoinflammatory keratinization diseases" (AIKD) has been proposed. AIKD encompasses diseases with mixed pathomechanisms of autoinflammation and autoimmunity, and includes IL-36 receptor antagonist (IL-36Ra)-related pustulosis, CARD14-mediated pustular psoriasis, pityriasis rubra pilaris (PRP) type V, and familial keratosis lichenoides chronica (KLC)...
February 1, 2018: Journal of Dermatological Science
https://www.readbyqxmd.com/read/29416822/il-36-cytokines-in-autoimmunity-and-inflammatory-disease
#3
REVIEW
Liping Ding, Xiaohui Wang, Xiaoping Hong, Liwei Lu, Dongzhou Liu
The inteleukin-36 (IL-36) cytokines include IL-36α, IL-36β, IL-36γ and IL-36Ra, which belong to the IL-1 family and exert pro-inflammatory effects on various target cells such as keratinocytes, synoviocytes, dendritic cells and T cells. Emerging evidence has suggested a role of IL-36 in the pathogenesis of many inflammatory diseases. Here, we provide a brief review on the activation of IL-36 family cytokines and their involvement in autoimmunity and inflammatory diseases, which will provide further insights in understanding the functions of IL-36 family cytokines in the pathophysiology of autoimmunity and inflammatory diseases...
January 5, 2018: Oncotarget
https://www.readbyqxmd.com/read/29367626/il-36-lxr-axis-modulates-cholesterol-metabolism-and-immune-defense-to-mycobacterium-tuberculosis
#4
Fadhil Ahsan, Jeroen Maertzdorf, Ute Guhlich-Bornhof, Stefan H E Kaufmann, Pedro Moura-Alves
Mycobacterium tuberculosis (Mtb) is a life-threatening pathogen in humans. Bacterial infection of macrophages usually triggers strong innate immune mechanisms, including IL-1 cytokine secretion. The newer member of the IL-1 family, IL-36, was recently shown to be involved in cellular defense against Mtb. To unveil the underlying mechanism of IL-36 induced antibacterial activity, we analyzed its role in the regulation of cholesterol metabolism, together with the involvement of Liver X Receptor (LXR) in this process...
January 24, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29344110/anti-interleukin-and-interleukin-therapies-for-psoriasis-current-evidence-and-clinical-usefulness
#5
REVIEW
Ya-Chu Tsai, Tsen-Fang Tsai
Anti-interleukin (IL) therapies have emerged as a major treatment for patients with moderate-to-severe psoriasis. This article reviews the up-to-date results of pivotal clinical trials targeting the interleukins used for the treatment of psoriasis, including IL-1, IL-2, IL-6, IL-8, IL-10, IL-12, IL-17, IL-20, IL-22, IL-23, IL-36 and bispecific biologics IL-17A/tumor necrosis factor alpha (TNF-α). Cytokines involved in the circuits of psoriasis inflammation without ongoing clinical trials are also mentioned (IL-9, IL-13, IL-15, IL-16, IL-18, IL-19, IL-21, IL-24, IL-27, IL-33, IL-35, IL-37, and IL-38)...
November 2017: Therapeutic Advances in Musculoskeletal Disease
https://www.readbyqxmd.com/read/29339122/regnase-1-an-immuno-modulator-limits-the-il-36-il-36r-auto-stimulatory-loop-in-keratinocytes-to-suppress-skin-inflammation
#6
Mikiro Takaishi, Takashi Satoh, Shizuo Akira, Shigetoshi Sano
No abstract text is available yet for this article.
January 12, 2018: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/29305258/irf-2-haploinsufficiency-causes-enhanced-imiquimod-induced-psoriasis-like-skin-inflammation
#7
Makiko Kawaguchi, Tomonori Oka, Makoto Sugaya, Hiraku Suga, Takayuki Kimura, Sohshi Morimura, Hideki Fujita, Shinichi Sato
BACKGROUNDS: IFN regulatory factor (IRF)-2 is one of the potential susceptibility genes for psoriasis, but how this gene influences psoriasis pathogenesis is unclear. Topical application of imiquimod (IMQ), a TLR7 ligand, induces psoriasis-like skin lesions in mice. OBJECTIVE: The aim of this study was to investigate whether IRF-2 gene status would influence severity of skin disease in IMQ-treated mice. METHODS: Imiquimod-induced psoriasis-like skin inflammation was assessed by clinical findings, histology, and cytokine expression...
December 28, 2017: Journal of Dermatological Science
https://www.readbyqxmd.com/read/29288651/unopposed-il-36-activity-promotes-clonal-cd4-t-cell-responses-with-il-17a-production-in-generalized-pustular-psoriasis
#8
Akiko Arakawa, Sigrid Vollmer, Petra Besgen, Adrian Galinski, Burkhard Summer, Yoshio Kawakami, Andreas Wollenberg, Klaus Dornmair, Michael Spannagl, Thomas Ruzicka, Peter Thomas, Jörg C Prinz
Generalized pustular psoriasis (GPP) is the most severe psoriasis variant. Mutations in the IL-36 antagonist IL36RN, in CARD14 or AP1S3 provide genetic evidence for autoinflammatory aetiology but cannot explain its pathogenesis completely. Here we demonstrate that unopposed IL-36 signalling promotes antigen-driven and likely pathogenic T-helper 17 (Th17) responses in GPP. We observed that CD4+ T cells in blood and skin lesions of GPP patients were characterized by intense hyperproliferation, production of the GPP key mediator, IL-17A, and highly restricted T-cell receptor (TCR) repertoires with identical T-cell clones in blood and skin lesions indicating antigen-driven T-cell expansions...
December 27, 2017: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/29274415/the-activation-and-function-of-il-36%C3%AE-in-neutrophilic-inflammation-in-chronic-rhinosinusitis
#9
Hai Wang, Zhi-Yong Li, Wen-Xiu Jiang, Bo Liao, Guan-Ting Zhai, Nan Wang, Zhen Zhen, Jian-Wen Ruan, Xiao-Bo Long, Heng Wang, Wei-Hong Liu, Geng-Tian Liang, Wei-Min Xu, Atsushi Kato, Zheng Liu
BACKGROUND: Although increased accumulation of neutrophils has been noted in chronic rhinosinusitis (CRS), the function and regulation of neutrophils in CRS are largely unknown. IL-36 family cytokines may play an important role in neutrophilic inflammation. OBJECTIVE: To investigate the expression and function of IL-36 cytokines in CRS. METHODS: Quantitative RT-PCR, immunohistochemistry, immunofluorescence, and ELISA were used to investigate the expression of IL-36 cytokines and IL-36 receptor (IL-36R) in sinonasal mucosa...
December 20, 2017: Journal of Allergy and Clinical Immunology
https://www.readbyqxmd.com/read/29247994/regulation-and-function-of-interleukin-36-cytokines
#10
REVIEW
Esen Yonca Bassoy, Jennifer E Towne, Cem Gabay
The interleukin (IL)-36 cytokines include 3 agonists, IL-36α, IL-36β, and IL-36γ that bind to a common receptor composed of IL-36R and IL-1RAcP to stimulate inflammatory responses. IL-36Ra is a natural antagonist that binds to IL-36R, but does not recruit the co-receptor IL-1RAcP and does not stimulate any intracellular responses. The IL-36 cytokines are expressed predominantly by epithelial cells and act on a number of cells including immune cells, epithelial cells, and fibroblasts. Processing of the N-terminus is required for full agonist or antagonist activity for all IL-36 members...
January 2018: Immunological Reviews
https://www.readbyqxmd.com/read/29247986/biology-of-il-38-and-its-role-in-disease
#11
REVIEW
Frank L van de Veerdonk, Dennis M de Graaf, Leo Ab Joosten, Charles A Dinarello
IL-38 belongs to the IL-36 cytokines, which in turn are part of the IL-1 family. The first biological function of IL-38 described was blocking the activation of the IL-36R signaling similar to IL-36Ra. Since IL-36 cytokines require processing in order to become fully active, it is likely that IL-38 also must be processed to become maximally active. However, the protease(s) responsible for this is currently not known. In addition of IL-38 binding IL-36R, it has been proposed it can also interact with the co-receptor TIGIRR2...
January 2018: Immunological Reviews
https://www.readbyqxmd.com/read/29246798/dlx3-dependent-stat3-signaling-in-keratinocytes-regulates-skin-immune-homeostasis
#12
Shreya Bhattacharya, Jin-Chul Kim, Youichi Ogawa, Gaku Nakato, Veronica Nagle, Stephen R Brooks, Mark C Udey, Maria I Morasso
Epidermal specific deletion of the homeobox transcription regulator DLX3 disrupts keratinocyte differentiation and results in an IL-17-linked psoriasis-like skin inflammation. To identify the epidermal initiating signals produced by DLX3-null keratinocytes, we performed acute deletion of DLX3 in adult epidermis using a tamoxifen-inducible Krt14-cre/ERT system. K14CreERT;DLX3fl/fl (icKO) skin exhibited dysregulated expression of differentiation-associated genes, upregulation of proinflammatory cytokines, and accumulation of Langerhans cells and macrophages within 3 days of tamoxifen-induced DLX3 ablation...
December 12, 2017: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/29241623/knockout-of-the-interleukin-36-receptor-protects-against-renal-ischemia-reperfusion-injury-by-reduction-of-proinflammatory-cytokines
#13
Hirofumi Nishikawa, Yoshinori Taniguchi, Tatsuki Matsumoto, Naoki Arima, Mamoru Masaki, Yoshiko Shimamura, Kosuke Inoue, Taro Horino, Shimpei Fujimoto, Kentaro Ohko, Toshihiro Komatsu, Keiko Udaka, Shigetoshi Sano, Yoshio Terada
IL-36, a newly named member of the IL-1 cytokine family, includes 3 isoforms, IL-36α, IL-36β, and IL-36γ, all of which bind to a heterodimer containing the IL-36 receptor (IL-36R). Little is known about the role of the IL-36 axis in acute kidney injury (AKI) pathogenesis. Therefore, we evaluated IL-36 function in the bilateral renal ischemia-reperfusion injury model of AKI using IL-36R knockout and wild-type mice. IL-36R was found to be expressed in the kidney, mainly in proximal tubules. In IL-36R knockout mice, plasma creatinine, blood urea nitrogen, and IL-6 levels after ischemia-reperfusion injury were significantly lower than those in wild-type mice...
December 11, 2017: Kidney International
https://www.readbyqxmd.com/read/29237761/erratum-for-the-research-article-an-analysis-of-il-36-signature-genes-and-individuals-with-il1rl2-knockout-mutations-validates-il-36-as-a-psoriasis-therapeutic-target-by-s-k-mahil-m-catapano-p-di-meglio-n-dand-h-ahlfors-i-m-carr-c-h-smith-r-c-trembath-m-peakman
#14
https://www.readbyqxmd.com/read/29203183/the-il-1-family-of-cytokines-do-they-have-a-role-in-scleroderma-fibrosis
#15
REVIEW
Carol M Artlett
Systemic sclerosis is a profibrotic autoimmune disease mediated by the dysregulation in collagen synthesis, leading to the increased deposition of collagens, primarily type I and III, and the deposition of other extracellular matrix proteins in the skin and internal organs, in a mechanism that is thought to be an over active wound healing process. These patients experience significant morbidity and the mortality rate in this disease is high. Indeed, scleroderma is the most deadly of diseases in the autoimmune spectrum...
December 4, 2017: Immunology Letters
https://www.readbyqxmd.com/read/29198612/il-1-family-cytokines-in-cardiovascular-disease
#16
Susanne Pfeiler, Holger Winkels, Malte Kelm, Norbert Gerdes
The interleukin (IL)-1 family is a group of cytokines crucially involved in regulating immune responses to infectious challenges and sterile insults. The family consists of the eponymous pair IL-1α and IL-1β, IL-18, IL-33, IL-37, IL-38, and several isoforms of IL-36. In addition, two endogenous inhibitors of functional receptor binding, IL-1R antagonist (IL-1Ra) and IL-36Ra complete the family. To gain biological activity IL-1β and IL-18 require processing by the protease caspase-1 which is associated with the multi-protein complex inflammasome...
November 30, 2017: Cytokine
https://www.readbyqxmd.com/read/29186830/the-genetic-basis-of-psoriasis
#17
REVIEW
Francesca Capon
Psoriasis is widely regarded as a multifactorial condition which is caused by the interaction between inherited susceptibility alleles and environmental triggers. In the last decade, technological advances have enabled substantial progress in the understanding of disease genetics. Genome-wide association studies have identified more than 60 disease susceptibility regions, highlighting the pathogenic involvement of genes related to Th17 cell activation. This pathway has now been targeted by a new generation of biologics that have shown great efficacy in clinical trials...
November 25, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29180446/quantitative-ligand-and-receptor-binding-studies-reveal-the-mechanism-of-interleukin-36-il-36-pathway-activation
#18
Li Zhou, Viktor Todorovic, Steve Kakavas, Bernhard Sielaff, Limary Medina, Leyu Wang, Ramkrishna Sadhukhan, Henning Stockmann, Paul L Richardson, Enrico DiGiammarino, Chaohong Sun, Victoria Scott
IL-36 cytokines signal through the IL-36 re-ceptor (IL-36R) and a shared subunit, IL-1 receptor accessory protein (IL-1RAcP). The activation mechanism for the IL-36 pathway is proposed to be similar to that of IL-1 in that an IL-36R agonist (IL-36α, IL-36β, or IL-36γ) forms a binary complex with IL-36R, which then recruits IL-1RAcP. Recent studies have shown that IL-36R interacts with IL-1RAcP even in the absence of an agonist. To elucidate the IL-36 activation mechanism, we considered all possible binding events for IL-36 ligands/receptors and examined these events in direct binding assays...
November 27, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29170040/elevated-production-of-il-36%C3%AE-in-chronic-hepatitis-b-virus-infected-patients-correlates-with-viral-load
#19
Yi Gong, Zhan Tingxi, Li Qing, Zhang Guozhen, Tan Bing, Yang Xiaoliang, Wu Yan, Jue Wenjuan, Xing Yan, Liu Hui, Hu Xue, Yu Zebo
Chronic hepatitis B (CHB) infection is a typical inflammatory disease characterized by a dysregulated expression of cytokines, which contributes to the pathogenesis of chronic Hepatitis B virus (HBV) infection. IL-36 cytokines (IL-36α, IL-36β, IL-36γ and IL-36Ra) are important players in infection and immunity. However, their roles in the pathogenesis of chronic HBV infection remain unknown. Here the circulating concentrations of IL-36 cytokines from 50 CHB patients and 30 healthy controls were determined by enzyme-linked immunosorbent assay (ELISA)...
November 20, 2017: Microbial Pathogenesis
https://www.readbyqxmd.com/read/29166668/interleukin-36%C3%AE-and-il-36-receptor-signaling-mediate-impaired-host-immunity-and-lung-injury-in-cytotoxic-pseudomonas-aeruginosa-pulmonary-infection-role-of-prostaglandin-e2
#20
Tetsuji Aoyagi, Michael W Newstead, Xianying Zeng, Yuta Nanjo, Marc Peters-Golden, Mitsuo Kaku, Theodore J Standiford
Pseudomonas aeruginosa is a Gram-negative pathogen that can lead to severe infection associated with lung injury and high mortality. The interleukin (IL)-36 cytokines (IL-36α, IL-36β and IL-36γ) are newly described IL-1 like family cytokines that promote inflammatory response via binding to the IL-36 receptor (IL-36R). Here we investigated the functional role of IL-36 cytokines in the modulating of innate immune response against P. aeruginosa pulmonary infection. The intratracheal administration of flagellated cytotoxic P...
November 22, 2017: PLoS Pathogens
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