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IL-36

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https://www.readbyqxmd.com/read/29655629/intramuscular-vaccination-of-guinea-pigs-with-the-live-attenuated-human-herpes-simplex-vaccine-vc2-stimulates-a-transcriptional-profile-of-vaginal-th17-and-regulatory-tr1-responses
#1
Brent A Stanfield, Paul J F Rider, John Caskey, Fabio Del Piero, Konstantin G Kousoulas
Herpes simplex virus is a common causative agent of oral and genital diseases. Novel vaccines and therapeutics are needed to combat herpes infections especially after the failure of subunit vaccines in human clinical trials. We have shown that the live-attenuated HSV-1 VC2 vaccine strain is unable to establish latency in vaccinated animals and produces a robust immune response capable of completely protecting mice against lethal vaginal HSV-1 or HSV-2 infections. The guinea pig represents the best small animal model of genital HSV-2 disease...
April 11, 2018: Vaccine
https://www.readbyqxmd.com/read/29644902/interleukin-il-36-gamma-induces-mucin-5ac-oligomeric-mucus-gel-forming-expression-via-il-36-receptor-extracellular-signal-regulated-kinase-1-and-2-and-p38-nuclear-factor-kappa-light-chain-enhancer-of-activated-b-cells-in-human-airway-epithelial-cells
#2
Chang Hoon Bae, Yoon Seok Choi, Hyung Gyun Na, Si-Youn Song, Yong-Dae Kim
BACKGROUND: Mucin 5AC, oligomeric mucus/gel-forming (MUC5AC) expression is significantly increased in allergic and inflammatory airway diseases. Interleukin (IL) 36 gamma is predominantly expressed in airway epithelial cells and plays an important role in innate and adaptive immune responses. IL-36 gamma is induced by many inflammatory mediators, including cytokines and bacterial and viral infections. However, the association between IL-36 gamma and mucin secretion in human airway epithelial cells has not yet been fully investigated...
March 2018: American Journal of Rhinology & Allergy
https://www.readbyqxmd.com/read/29571080/increased-serum-il-36%C3%AE-and-il-36%C3%AE-levels-in-patients-with-systemic-lupus-erythematosus-association-with-disease-activity-and-arthritis
#3
Shao-Zhen Mai, Chi-Jun Li, Xiao-Ying Xie, Hui Xiong, Min Xu, Fan-Qin Zeng, Qing Guo, Yan-Fang Han
IL-36 cytokines (IL-36Ra, IL-36α, IL-36β and IL-36γ) belong to the IL-1 family and have been linked to several autoimmune diseases. However, little is known about the relationships between systemic lupus erythematosus (SLE) and IL-36 cytokines. In this study, serum IL-36 cytokine levels were determined by enzyme-linked immunosorbent assay (ELISA), and their associations with SLE-related parameters were analyzed in 72 SLE patients and 63 healthy controls. Additionally, IL-36 cytokine mRNA levels were assessed in 30 of 72 SLE patients and 20 of 63 healthy controls using real-time quantitative reverse transcription polymerase chain reaction (RT-PCR)...
March 20, 2018: International Immunopharmacology
https://www.readbyqxmd.com/read/29565192/pharmacotherapeutic-approaches-for-treating-psoriasis-in-difficult-to-treat-areas
#4
Dario Kivelevitch, Jillian Frieder, Ian Watson, So Yeon Paek, M Alan Menter
Despite great therapeutic advancements in psoriasis, four notable difficult-to-treat areas including the scalp, nails, intertriginous (including genitals), and palmoplantar regions, pose a challenge to both physicians and patients. Localized disease of these specific body regions inflicts a significant burden on patients' quality of life and requires an adequate selection of treatments. Areas covered: This manuscript discusses appropriate therapies and important treatment considerations for these difficult-to-treat areas based on the available clinical data from the literature...
March 22, 2018: Expert Opinion on Pharmacotherapy
https://www.readbyqxmd.com/read/29554104/the-severity-of-imiquimod-induced-mouse-skin-inflammation-is-independent-of-endogenous-il-38-expression
#5
Jennifer Palomo, Sabina Troccaz, Dominique Talabot-Ayer, Emiliana Rodriguez, Gaby Palmer
The IL-1 cytokine family includes eleven members, among which Il-36α, β and γ, IL-36Ra and IL-38. The IL-36 cytokines are involved in the pathogenesis of psoriasis. IL-38 is also expressed in the skin and was previously proposed to act as an IL-36 antagonist. In this study, we thus examined expression and function of Il-38 in a mouse model of imiquimod (IMQ)-induced skin inflammation. Il-38 mRNA was detected in the epidermis and in primary mouse keratinocytes, but not in dermal fibroblasts. At the peak of IMQ-induced inflammation, skin Il-38 mRNA levels were reduced, whereas Il-36ra mRNA expression increased...
2018: PloS One
https://www.readbyqxmd.com/read/29539422/extracellular-neutrophil-proteases-are-efficient-regulators-of-il-1-il-33-and-il-36-cytokine-activity-but-poor-effectors-of-microbial-killing
#6
Danielle M Clancy, Graeme P Sullivan, Hannah B T Moran, Conor M Henry, Emer P Reeves, Noel G McElvaney, Ed C Lavelle, Seamus J Martin
Neutrophil granule proteases are thought to function as anti-microbial effectors, cooperatively hydrolyzing microorganisms within phagosomes, or upon deployment into the extracellular space. However, evidence also suggests that neutrophil proteases play an important role in the coordination and escalation of inflammatory reactions, but how this is achieved has been obscure. IL-1 family cytokines are important initiators of inflammation and are typically released via necrosis but require proteolytic processing for activation...
March 13, 2018: Cell Reports
https://www.readbyqxmd.com/read/29515113/suppressing-il-36-driven-inflammation-using-peptide-pseudosubstrates-for-neutrophil-proteases
#7
Graeme P Sullivan, Conor M Henry, Danielle M Clancy, Tazhir Mametnabiev, Ekaterina Belotcerkovskaya, Pavel Davidovich, Sylvia Sura-Trueba, Alexander V Garabadzhiu, Seamus J Martin
Sterile inflammation is initiated by molecules released from necrotic cells, called damage-associated molecular patterns (DAMPs). Members of the extended IL-1 cytokine family are important DAMPs, are typically only released through necrosis, and require limited proteolytic processing for activation. The IL-1 family cytokines, IL-36α, IL-36β, and IL-36γ, are expressed as inactive precursors and have been implicated as key initiators of psoriatic-type skin inflammation. We have recently found that IL-36 family cytokines are proteolytically processed and activated by the neutrophil granule-derived proteases, elastase, and cathepsin G...
March 7, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29474749/mek-erk-signaling-diametrically-controls-the-stimulation-of-il-23p19-and-ebi3-expression-in-epithelial-cells-by-il-36%C3%AE
#8
Glen M Scholz, Jacqueline E Heath, Katrina A Walsh, Eric C Reynolds
Interleukin (IL)-36 cytokines are important regulators of mucosal homeostasis and inflammation. We previously established that oral epithelial cells strongly upregulate IL-36γ expression in response to the bacterial pathogen Porphyromonas gingivalis. Here, we have established that IL-36γ stimulates the expression of the IL-12 cytokine family members, IL-23p19 and Epstein-Barr Virus-Induced Gene 3 (EBI3), by oral epithelial cells; their expression was also selectively stimulated by IL-36α. Notably, IL-23p19 and EBI3 expression was not stimulated by P...
February 23, 2018: Immunology and Cell Biology
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
#9
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
#10
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
#11
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
#12
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
#13
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-immunomodulator-limits-the-il-36-il-36r-autostimulatory-loop-in-keratinocytes-to-suppress-skin-inflammation
#14
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
#15
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...
April 2018: 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
#16
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 etiology but cannot explain its pathogenesis completely. Here we demonstrate that unopposed IL-36 signaling promotes antigen-driven and likely pathogenic T-helper type 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 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
#17
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: This study sought 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 21, 2017: Journal of Allergy and Clinical Immunology
https://www.readbyqxmd.com/read/29247994/regulation-and-function-of-interleukin-36-cytokines
#18
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
#19
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
#20
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 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
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