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Full-length and N-terminally truncated recombinant interleukin-38 variants are similarly inefficient in antagonizing interleukin-36 and interleukin-1 receptors.
Cell Commun Signal
January 2025
Division of Rheumatology, Department of Medicine, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Background: Interleukin (IL)-38 is an IL-1 family cytokine that was proposed to exert anti-inflammatory effects. However, its mechanisms of action are not well understood and the identity of the IL-38 receptor(s) remains debated. Proposed candidates include the IL-1 receptor (IL-1R1), the IL-36 receptor (IL-36R) and the orphan receptor IL-1RAPL1.
View Article and Find Full Text PDFGeneralized pustular psoriasis: immunological mechanisms, genetics, and emerging therapeutics.
Trends Immunol
January 2025
College of Medicine, Chang Gung University, Taoyuan, Taiwan; Department of Dermatology, Chang Gung Memorial Hospital, Keelung, Taiwan; Department of Dermatology, Chang Gung Memorial Hospital, Linkou, Taiwan; Department of Dermatology, Chang Gung Memorial Hospital, Taipei, Taiwan; Department of Dermatology, Drug Hypersensitivity Clinical and Research Center, Chang Gung Memorial Hospital, Linkou, Taiwan; Cancer Vaccine and Immune Cell Therapy Core Laboratory, Department of Medical Research, Chang Gung Memorial Hospital, Linkou, Taiwan; Chang Gung Immunology Consortium, Chang Gung Memorial Hospital and Chang Gung University, Taoyuan, Taiwan; Department of Dermatology, Xiamen Chang Gung Hospital, Xiamen, China; Xiamen Chang Gung Allergology Consortium, Xiamen Chang Gung Hospital, Xiamen, China; Graduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan; Immune-Oncology Center of Excellence, Chang Gung Memorial Hospital, Linkou, Taiwan; Whole-Genome Research Core Laboratory of Human Diseases, Chang Gung Memorial Hospital, Keelung, Taiwan; Genomic Medicine Core Laboratory, Chang Gung Memorial Hospital, Linkou, Taiwan; School of Medicine, National Tsing Hua University, Hsinchu, Taiwan. Electronic address:
Generalized pustular psoriasis (GPP) is a rare human autoinflammatory disorder with life-threatening systemic effects. Keratinocyte-derived interleukin (IL)-36 signaling has been identified as a key mediator of immune response in the skin of affected individuals. Recognition of various mutations along the IL-36 axis and the downstream nuclear transcription factor κB (NF-κB) signaling have established GPP as genetically, immunologically, and histopathologically distinct and amenable to immunomodulation, which is epitomized by the recent success of IL-36 antagonism.
View Article and Find Full Text PDFThe Association of Interleukin-36 Staining Intensity and Response to Biologic Therapy in Patients With Psoriasis: A Retrospective Immunohistochemical and Chart Review Pilot Study.
J Cutan Pathol
January 2025
Department of Dermatology, University of California, San Francisco, California, USA.
Background: There are limited surrogate biomarkers to identify the active inflammatory pathway in psoriasis to direct treatment with targeted biologic therapies. We investigated the association of interleukin (IL)-36 epidermal expression, a diagnostic marker of psoriasis, with response to biologic therapy in patients with psoriasis.
Methods: Retrospective immunohistochemical and chart review pilot study.
Spesolimab, the first-in-class anti-IL-36R antibody: From bench to clinic.
J Dermatol
November 2024
Division of Cutaneous Science, Department of Dermatology, Nihon University School of Medicine, Tokyo, Japan.
Article Synopsis
- Inflammatory diseases linked to pro-inflammatory cytokines have led to targeted therapies, with IL-36 cytokines being significant in conditions like generalized pustular psoriasis (GPP) and others.
- The IL-36R-targeting antibody spesolimab shows promise, effectively inhibiting IL-36R signaling and presenting a favorable safety profile in multiple studies.
- Clinical trials highlight spesolimab's ability to improve symptoms and quality of life for GPP patients, while ongoing research continues to explore its efficacy in other related diseases like palmoplantar pustulosis and Netherton syndrome.
Casting NETs on Psoriasis: The modulation of inflammatory feedback targeting IL-36/IL-36R axis.
Int Immunopharmacol
December 2024
Key Laboratory of Traditional Chinese Korean Medicine Research of State Ethnic Affairs Commission, College of Pharmacy, Yanbian University, Yanji, Jilin Province 133002, China; Key Laboratory of Natural Medicines of the Changbai Mountain, Ministry of Education, College of Pharmacy, Yanbian University, Yanji, Jilin Province 133002, China. Electronic address:
NETosis happens when neutrophils are activated and neutrophil extracellular traps (NETs) are formed synchronously, which is a hallmark of psoriasis. However, the specific trigger that drives NET formation and the distinct contents and interaction with interleukin-36 receptor (IL-36R) of NETs remain to be further elucidated. This work identified NET formation driven by toll-like receptor (TLR) 3 ligand (especially polyinosinic-polycytidylic acid (Poly(I:C)) were enhanced by purinergic receptor P2X ligand-gated ion channel 7 receptor (P2X7R) ligands (especially adenosine 5'-triphosphate (ATP)).
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