Last update 01 Nov 2024

IL-20 receptor

Last update 01 Nov 2024

Basic Info

Synonyms-

Introduction-

Drugs associated with IL-20 receptor

MT204

Target

IL-20 receptor

Mechanism

IL-20 receptor inhibitors

Active Org.

Amgen Rockville, Inc.

Originator Org.

Amgen Rockville, Inc.

Active Indication

Autoimmune Diseases

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

HG-1330

Target

IL-20 receptor

Mechanism

IL-20 receptor modulators

Active Org.-

Originator Org.

Human Genome Sciences, Inc.

Active Indication-

Inactive Indication

Immune System Diseases [+1]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with IL-20 receptor

100 Translational Medicine associated with IL-20 receptor

0 Patents (Medical) associated with IL-20 receptor

126

Literatures (Medical) associated with IL-20 receptor

01 Sep 2024·Journal of Interferon & Cytokine Research

Deciphering the Receptor-Mediated Signaling Pathways of Interleukin-19 and Interleukin-20

Review

Author: Devasahayam Arokia Balaya, Rex ; George, Mejo ; Prasad, Ganesh ; Sanjeev, Diya ; Kanekar, Saptami ; Keshava Prasad, Thottethodi Subrahmanya ; Raju, Rajesh ; Dagamajalu, Shobha ; Shaji, Vineetha

Interleukin-19 (IL-19) and Interleukin-20 (IL-20) are inflammatory cytokines belonging to the IL-10 family with immunoregulatory properties. Emerging evidence highlights the importance of association of these cytokines with both immunological and inflammatory disorders, including chronic inflammation, cardiac dysfunction, and cancer. IL-19 and IL-20 bind to the heterodimeric receptor complex and induce multiple downstream signaling cascades by activating the signal transducer and activator of transcription 3 (STAT3), Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), AKT serine/threonine kinase 1 (AKT1), and NFKB inhibitor alpha (NFKBIA), leading to proinflammatory and anti-inflammatory reactions in cancer, inflammation, tumor microenvironment, and infectious diseases. Considering the significant role of these cytokines, we integrated its cellular signaling network by combining multiomics molecular events associated with 56 molecules of induced by IL-19 and 156 molecules of by IL-20. The reactions of these signaling events are classified into enzyme catalysis/post-translational modifications, activation/inhibition events, molecular associations, gene regulations at the mRNA and protein level, and the protein translocation events. We believe that this signaling pathway map would serve as a knowledge base, that aid researchers and clinicians to understand and explore the intricate mechanisms and identify novel signaling components and therapeutic targets for diseases associated with dysregulated IL-19 and IL-20 signaling.

01 Jun 2024·Journal of Periodontal Research

The effect of interleukin‐20 on periodontal tissue destruction in individuals with periodontitis

Article

Author: Yılmaz, A ; Yemenoglu, H ; Senkal, R ; Kose, O ; Mataracı Karakaş, S ; Akyıldız, K

AbstractBackground and ObjectivePeriodontitis is an inflammatory disease that destroys periodontal tissues. Interleukin‐20 (IL‐20), on the other hand, is known as a potent angiogenic, chemotactic, and pro‐inflammatory cytokine associated with various chronic inflammatory disorders. IL‐20 has a significant role in the regulation of osteoclastogenesis and osteoblastogenesis. This study aimed to evaluate the effect of IL‐20 on periodontal destruction.MethodsIn this study, a total of 60 participants were included, 30 of whom were systemically and periodontally healthy (control group), and 30 were systemically healthy but had periodontitis (periodontitis group). Gingival crevicular fluid (GCF) and serum samples were collected from the participants for biochemical analysis. Enzyme‐linked immunosorbent assay was used to determine the levels of IL‐20, tumor necrosis factor (TNF)‐α, IL1β/IL‐10, RANKL/osteoprotegerin (OPG), and matrix metalloproteinase‐8 (MMP8). For statistical analysis, the independent t‐test, Pearson correlation coefficients, and the Chi‐square test were used.ResultsGCF IL‐20, RANKL, RANKL/OPG, serum IL‐20, RANKL, RANKL/OPG, MMP‐8, TNF‐α, IL‐1B, and IL‐1β/IL‐10 values were found to be statistically significantly higher in the periodontitis group than in the control group. GCF OPG and serum IL‐10 values were found to be statistically significantly higher in the control group than in the periodontitis group. No statistically significant difference was observed between the groups in serum OPG values. A statistically significantly positive correlation was observed between serum IL‐20 value and serum RANKL, RANKL/OPG, MMP‐8, TNF‐α, IL‐1β values, and periodontal clinical parameters. The ROC curves showed: AUC = 0.788 for GCF IL‐20, and AUC = 1.000 for serum IL‐20.ConclusionAccording to the results of the study, IL‐20 was found to be associated with periodontitis. The role of IL‐20 in periodontal pathogenesis is related to osteoclastogenesis and collagen degradation. It is conceivable that IL‐20 may increase bone destruction by both affecting the RANKL/OPG ratio and proinflammatory cytokines.

01 Feb 2024·Gut

IL-20 controls resolution of experimental colitis by regulating epithelial IFN/STAT2 signalling

Article

Author: Becker, Christoph ; Trajanoski, Zlatko ; Gonzalez-Acera, Miguel ; Hartmann, Arndt ; Zundler, Sebastian ; Gamez-Belmonte, Reyes ; Schickedanz, Laura ; Hracsko, Zsuzsanna ; Siegmund, Britta ; Atreya, Raja ; Stolzer, Iris ; Finotto, Susetta ; Siebler, Jürgen ; Günther, Claudia ; Wirtz, Stefan ; Neurath, Markus F ; Dressel, Anja ; Sturm, Gregor ; Chiriac, Mircea Teodor ; Rath, Timo ; Wittner, Leonie ; Vetrano, Stefania ; Danese, Silvio ; Hundorfean, Gheorghe ; Kühl, Anja A ; Erkert, Lena

ObjectiveWe sought to investigate the role of interleukin (IL)-20 in IBD and experimental colitis.DesignExperimental colitis was induced in mice deficient in components of the IL-20 and signal transducer and activator of transcription (STAT)2 signalling pathways. In vivo imaging, high-resolution mini-endoscopy and histology were used to assess intestinal inflammation. We further used RNA-sequencing (RNA-Seq), RNAScope and Gene Ontology analysis, western blot analysis and co-immunoprecipitation, confocal microscopy and intestinal epithelial cell (IEC)-derived three-dimensional organoids to investigate the underlying molecular mechanisms. Results were validated using samples from patients with IBD and non-IBD control subjects by a combination of RNA-Seq, organoids and immunostainings.ResultsIn IBD,IL20levels were induced during remission and were significantly higher in antitumour necrosis factor responders versus non-responders. IL-20RA and IL-20RB were present on IECs from patients with IBD and IL-20-induced STAT3 and suppressed interferon (IFN)-STAT2 signalling in these cells. In IBD, experimental dextran sulfate sodium (DSS)-induced colitis and mucosal healing, IECs were the main producers of IL-20. Compared with wildtype controls,Il20−/−, Il20ra−/−andIl20rb−/−mice were more susceptible to experimental DSS-induced colitis. IL-20 deficiency was associated with increased IFN/STAT2 activity in mice and IFN/STAT2-induced necroptotic cell death in IEC-derived organoids could be markedly blocked by IL-20. Moreover, newly generatedStat2ΔIECmice, lacking STAT2 in IECs, were less susceptible to experimental colitis compared with wildtype controls and the administration of IL-20 suppressed colitis activity in wildtype animals.ConclusionIL-20 controls colitis and mucosal healing by interfering with the IFN/STAT2 death signalling pathway in IECs. These results indicate new directions for suppressing gut inflammation by modulating IL-20-controlled STAT2 signals.

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IL-20 receptor

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