ArticleJID innovations : skin science from molecules to population health2023
Tralokinumab Effectively Disrupts the IL-13/IL-13Rα1/IL-4Rα Signaling Complex but Not the IL-13/IL-13Rα2 Complex.
Article in JID innovations : skin science from molecules to population health, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Long-Term Disease Control and Minimal Disease Activity of Head and Neck Atopic Dermatitis in Patients Treated with Tralokinumab up to 4 Years.American journal of clinical dermatology · 2025Trial
- Tralokinumab Versus Dupilumab for the Treatment of Atopic Dermatitis with Moderate-to-Severe Hand Involvement: A Matching-Adjusted Indirect Comparison.Dermatology and therapy · 2026Article
- Real-World Efficacy and Systemic Immune Modulation Upon Tralokinumab Treatment in Atopic Dermatitis.Clinical and translational allergy · 2026Article
- A Response to: "Letter to the Editor Regarding 'Anchored Matching-Adjusted Indirect Comparison of the Long-Term Maintenance of Efficacy of Tralokinumab and Lebrikizumab in Patients with Moderate-to-Severe Atopic Dermatitis'".Dermatology and therapy · 2026Article
- Clinical Laboratory Parameters in Adolescents with Moderate-to-Severe Atopic Dermatitis Treated with Tralokinumab Up to Week 52 in the Phase 3 ECZTRA 6 Trial.Dermatology and therapy · 2026Article
- Long-Term Safety and Efficacy of Tralokinumab in Patients with Moderate-to-Severe Atopic Dermatitis Treated for up to 6 Years: Final Results from the Open-Label Extension Trial ECZTEND.Dermatology and therapy · 2026Article
- Immunomodulatory effects of nematode-microbiota interactions in cancer therapy.Frontiers in immunology · 2026Review
- Biologic Therapies Targeting Type 2 Signaling in Atopic Dermatitis: A Comparative Review of Structural and Thermodynamic Differences in Mechanism of Action.The Journal of investigative dermatology · 2025Review
- Clinically Meaningful Improvements in Adolescents with Moderate-to-Severe Atopic Dermatitis Treated with Tralokinumab who did not Achieve Clear or Almost Clear Skin at Week 16.Dermatology and therapy · 2025Article
- Cutaneous T Cell Lymphoma Following Dupilumab Therapy in Patients with Atopic Dermatitis: Clinical Review and Recommendations.American journal of clinical dermatology · 2025Review
- Article
- Biomarkers in Atopic Dermatitis: A Review of the Role of IL-13 and the Impact of Tralokinumab Treatment.American journal of clinical dermatology · 2025Review
- Type 2 Cytokine-Dependent Skin Barrier Regulation in Personalized 2-Dimensional and 3-Dimensional Skin Models of Atopic Dermatitis: A Pilot Study.JID innovations : skin science from molecules to population health · 2025Article
- Interleukin-13 Inhibitors in the Treatment of Atopic Dermatitis: The Role of Tralokinumab.Dermatology practical & conceptual · 2024Review
- Role of IL-4 and IL-13 in Cutaneous T Cell Lymphoma.Life (Basel, Switzerland) · 2024Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tralokinumab, a fully human mAb specifically targeting the IL-13 cytokine, has demonstrated clinical efficacy and safety in patients with moderate-to-severe atopic dermatitis. Tralokinumab binds IL-13 with high affinity, which prevents the interaction of IL-13 with IL-13Rα1 and subsequent signaling. Similarly, tralokinumab-bound IL-13 cannot bind to IL-13Rα2, a proposed decoy receptor that is reported to bind IL-13 with extraordinarily high affinity. It has however not been fully elucidated to what extent tralokinumab interferes with the endogenous regulation of IL-13 through IL-13Rα2. In this mechanistic study, we used biophysical, biochemical, and cellular assays to investigate the effect of tralokinumab on the interaction between IL-13 and IL-13Rα1 and IL-13Rα2, respectively, as well as the effects on IL-13Rα2-mediated IL-13 internalization. We demonstrate that IL-13Rα2 binds IL-13 with exceptionally high affinity and that tralokinumab is unable to displace IL-13 from IL-13Rα2. In contrast to this, tralokinumab is able to disrupt the IL-13/IL-13Rα1 and IL-13Rα1/IL-13/IL-4Rα complex. Furthermore, we demonstrate that whereas the IL-13/tralokinumab complex is unable to bind IL-13Rα2, any IL-13 that is not bound by tralokinumab (i.e., free IL-13) can be bound by IL-13Rα2 and subsequently internalized, regardless of the presence of tralokinumab. In summary, our study indicates that tralokinumab does not interfere with endogenous IL-13Rα2-mediated regulation of free IL-13.
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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.