Cited by 18Dermatology and Skin DiseasesAsthma and respiratory diseasesContact Dermatitis and Allergies

Biomarkers in Atopic Dermatitis: A Review of the Role of IL-13 and the Impact of Tralokinumab Treatment

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Gorelick, Joe, Nguyen, Andrea, Schneider, Shannon K R, Martel, Britta C., Madsen, Daniel E., Armstrong, April W.·2025·American Journal of Clinical Dermatology

Abstract

Atopic dermatitis (AD) is a chronic, inflammatory skin disease that can significantly affect quality of life. Presence, severity, and therapeutic response of AD are traditionally reported through clinical assessments including the Eczema Area and Severity Index or Investigator's Global Assessment. These clinical rating scales are visual assessments used in clinical trials to denotate AD severity. Alternatively, biomarkers open the potential to further enhance diagnosis of AD, assess disease status and severity, and potentially enable tailored treatment options for patients. Biomarkers can be classified according to their clinical use, clinical presentation, and underlying/endogenous molecular mechanisms. Specifically, interleukin (IL)-13, which has been shown to be a key biomarker in AD pathogenesis, can be used for prediction of AD development and to monitor clinical severity/response to treatment. Treatment with tralokinumab, a human monoclonal antibody that binds directly to-and subsequently blocks signaling of-IL-13, has been shown to reduce inflammation, re-balance the skin microbiome, and improve the skin barrier in patients with AD. In this review, key AD-related biomarkers, the role of IL-13 in driving AD pathogenesis, and the impact of IL-13 inhibition by tralokinumab on other AD-related biomarkers are discussed.

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Integrity signals

Registry

Crossref · 10.1007/s40257-024-00913-9

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  • Recent real-world evidence supports the effectiveness of JAK inhibitors in moderate-to-severe atopic dermatitis, particularly in patients with inadequate response to biologic therapies.

    “Recent real-world evidence further supports the effectiveness of JAK inhibitors in moderate-to-severe atopic dermatitis, particularly in patients with inadequate response to biologic therapies [11,16,17,18,19].”

    From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [19]

    The Conclusions and Future Perspectives section (page unavailable) reports that the JAK1 inhibitors upadacitinib and abrocitinib reduce AD-related biomarkers, supporting a narrower point about treatment response. It does not report real-world evidence of clinical effectiveness or outcomes in patients with inadequate responses to biologics; it says real-world biomarker studies are still needed. (LLM, conf=0.83)

    Experimental — accuracy not yet measured
  • Emerging strategies for atopic dermatitis include microbiome modulation, neuroimmune pathway targeting, and biomarker-guided treatment selection.

    “Emerging strategies include microbiome modulation, neuroimmune pathway targeting, and biomarker-guided treatment selection, reflecting an evolving precision medicine approach in atopic dermatitis.”

    From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [19]

    The Biomarkers in Atopic Dermatitis section says biomarkers may help distinguish beneficial treatments, and Conclusions and Future Perspectives links their assessment to treatment selection and precision medicine. The review also reports that tralokinumab improves the skin microbiome and discusses an itch-related pathway targeted by nemolizumab. It does not, however, present microbiome modulation as a distinct emerging treatment strategy; the microbiome effect it describes is likely indirect. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • IL-17 induces a pro-inflammatory state in keratinocytes, which then produce chemokines, cytokines, antimicrobial peptides, and growth factors that amplify leukocyte recruitment and epidermal remodeling.

    “IL-17 induces a pro-inflammatory state in keratinocytes, which in turn start producing chemokines, cytokines, antimicrobial peptides, and growth factors that amplify leukocyte recruitment and epidermal remodeling [18,19,20,21,22].”

    From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [19]

    In “IL-13 Drives Skin and Systemic Inflammation” (page unavailable), the review says IL-13 induces keratinocytes to secrete chemokines that attract immune cells. “IL-13 is Associated with Microbial Dysbiosis on the Skin” (page unavailable) also identifies keratinocytes as producers of antimicrobial peptides. The reviewed passages do not attribute this response to IL-17 or describe the full claimed sequence of cytokine and growth-factor production and epidermal remodeling. (LLM, conf=0.83)

    Experimental — accuracy not yet measured
  • IL-22 stimulates keratinocyte hyperplasia and abnormal differentiation, contributing to acanthosis, parakeratosis, and loss of the granular layer.

    “IL-22 will stimulate keratinocyte hyperplasia and abnormal differentiation, contributing to acanthosis, parakeratosis, and loss of the granular layer.”

    From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [19]

    The 'IL-13 Reduces Skin Barrier Integrity' section describes altered keratinocyte differentiation in atopic dermatitis, but attributes a role in barrier dysfunction to IL-13, not IL-22. Table 4 lists IL-22 as a biomarker reduced after tralokinumab treatment; it does not say IL-22 causes keratinocyte hyperplasia, acanthosis, parakeratosis, or loss of the granular layer. Searches for IL-22 and those histological terms found no passage establishing the claimed mechanism; page numbers were not available in our copy. (LLM, conf=0.76)

    Experimental — accuracy not yet measured
  • TNF-α, IL-17, and IL-22 magnify transcriptional responses in keratinocytes and endothelial cells.

    “TNF-α, IL-17, and IL-22 will magnify transcriptional responses in keratinocytes and endothelial cells.”

    From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [19]

    The section “IL-13 Drives Skin and Systemic Inflammation” (page unavailable) describes IL-13 inducing chemokine secretion by keratinocytes, not the claimed effect of TNF-α, IL-17, and IL-22. Searches for those cytokines, transcriptional responses, and endothelial cells found no passage addressing the claimed effect. (LLM, conf=0.75)

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Research works printed but not linked: 1

  1. [21]FDA-NIH Biomarker Working Group. BEST (Biomarkers, EndpointS, and other Tools). Resource [Internet]. Silver Spring (MD): Food and Drug Administration (US). Available from: https://www.ncbi.nlm.nih.gov/books/NBK326791/ Co-published by National Institutes of Health (US), Bethesda (MD); 2016. 27010052

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Authors
Gorelick, J., Nguyen, A., Schneider, S. K. R., Martel, B. C., Madsen, D. E., & Armstrong, A. W.
Affiliations
  • Leo Pharma (United States) (US)
  • Leo Pharma (Denmark) (DK)
  • University of California, Los Angeles (US)
Corresponding author
Gorelick, Joe
Venue
American Journal of Clinical Dermatology
Published
2025-01-16
Volume
26
Issue
2
Pages
199-211
ISSN
  • 1175-0561 (ISSN-L)
  • 1179-1888
OpenAlex
W4406429366
Cited by
18
References
69
Citations by year
2026: 9 · 2025: 9
FWCI
3.08
Type
journal article
Language
en
Open access
Locations
  • American Journal of Clinical Dermatology (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
Funders
LEO Pharma Inc
Topics
  • Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
  • Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
  • Health Sciences › Medicine › Dermatology › Contact Dermatitis and Allergies
Keywords
atopic dermatitis, biomarkers, IL-13, tralokinumab, IL-13 inhibition, disease severity assessment, skin microbiome, skin barrier, pathogenesis, monoclonal antibody therapy
MeSH terms
Antibodies, Monoclonal, Dermatitis, Atopic, Humans, Quality of Life, Severity of Illness Index, Skin, Biomarkers, Treatment Outcome, Interleukin-13

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