ArticlemAbs2017
Generation and functional characterization of anti-human and anti-mouse IL-36R antagonist monoclonal antibodies.
Article in mAbs, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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The trial behind it
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Who cites it
41 citing papers in PubMed, 85 citations in OpenAlex.
- Aged skin exacerbates experimental osteoarthritis via enhanced IL-36R signaling.Nature communications · 2026Article
- Epicutaneous Staphylococcus aureus initiates cross-tissue IL-36R signaling for neutrophilic lung inflammation in a model of the atopic march.Cell reports · 2025Article
- Article
- Biologics as a novel treatment option for palmoplantar pustulosis: a comprehensive review.Postepy dermatologii i alergologii · 2024Review
- FloxedCells · 2024Article
- Dual blockade of IL-17A and IL-36 pathways via a bispecific antibody exhibits enhanced anti-inflammatory potency.Frontiers in immunology · 2024Article
- Spesolimab Efficacy and Safety in Patients with Moderate-to-Severe Palmoplantar Pustulosis: A Multicentre, Double-Blind, Randomised, Placebo-Controlled, Phase IIb, Dose-Finding Study.Dermatology and therapy · 2023Article
- New insights on IL‑36 in intestinal inflammation and colorectal cancer (Review).Experimental and therapeutic medicine · 2023Review
- Targeting IL-36 in Inflammatory Skin Diseases.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2023Article
- Psoriasis: A Primer for General Physicians.Cureus · 2023Review
- The role of the interleukin-36 axis in generalized pustular psoriasis: a review of the mechanism of action of spesolimab.Frontiers in immunology · 2023Review
- IL-17A-driven psoriasis is critically dependent on IL-36 signaling.Frontiers in immunology · 2023Article
- Interleukin 36 receptor-inducible matrix metalloproteinase 13 mediates intestinal fibrosis.Frontiers in immunology · 2023Article
- Assessment of the Pharmacokinetics and Safety of Spesolimab, a Humanised Anti-interleukin-36 Receptor Monoclonal Antibody, in Healthy Non-Japanese and Japanese Subjects: Results from Phase I Clinical Studies.Clinical pharmacokinetics · 2022Article
- The Role of Interleukins in the Pathogenesis of Dermatological Immune-Mediated Diseases.Advances in therapy · 2022Review
- Plasma Levels of Interleukins 36α, 36β, and 37 in Patients with Psoriasis and Their Correlation with Disease Activity Parameters.Journal of clinical medicine · 2022Article
- Detection of cell markers from single cell RNA-seq with sc2marker.BMC bioinformatics · 2022Article
- IL-36 Cytokines: Their Roles in Asthma and Potential as a Therapeutic.Frontiers in immunology · 2022Review
- A Novel Antagonistic CD73 Antibody for Inhibition of the Immunosuppressive Adenosine Pathway.Molecular cancer therapeutics · 2021Article
- Exploring the Role of IL-36 Cytokines as a New Target in Psoriatic Disease.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
22 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deficiency of interleukin (IL)-36 receptor antagonist (DITRA) syndrome is a rare autosomal recessive disease caused by mutations in IL36RN. IL-36R is a cell surface receptor and a member of the IL1R family that is involved in inflammatory responses triggered in skin and other epithelial tissues. Accumulating evidence suggests that IL-36R signaling may play a role in the pathogenesis of psoriasis. Therapeutic intervention of IL-36R signaling offers an innovative treatment paradigm for targeting epithelial cell-mediated inflammatory diseases such as the life-threatening psoriasis variant called generalized pustular psoriasis (GPP). We report the discovery and characterization of MAB92, a potent, high affinity anti-human IL-36 receptor antagonistic antibody that blocks human IL-36 ligand (α, β and γ)-mediated signaling. In vitro treatment with MAB92 directly inhibits human IL-36R-mediated signaling and inflammatory cytokine production in primary human keratinocytes and dermal fibroblasts. MAB92 shows exquisite species specificity toward human IL-36R and does not cross react to murine IL-36R. To enable in vivo pharmacology studies, we developed a mouse cross-reactive antibody, MAB04, which exhibits overlapping binding and pharmacological activity as MAB92. Epitope mapping indicates that MAB92 and MAB04 bind primarily to domain-2 of the human and mouse IL-36R proteins, respectively. Treatment with MAB04 abrogates imiquimod and IL-36-mediated skin inflammation in the mouse, further supporting an important role for IL-36R signaling in epithelial cell-mediated inflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.