Lebrikizumab for the Treatment of Moderate-to-Severe Atopic Dermatitis
Open accessAbstract
Atopic dermatitis (AD) is a common, heterogeneous, inflammatory skin disorder characterized by chronic or relapsing eczematous lesions with intense pruritus and discomfort. Affected patients often experience significant impairment in their quality of life, and the treatment of moderate-to-severe AD forms remains challenging. In the past few decades, increasing knowledge on the AD pathogenesis has driven the development of novel targeted therapies. Interleukin (IL)-13 plays a central and pleiotropic role in AD pathogenesis, contributing directly or indirectly to epidermal barrier disfunction, type-2 inflammation, dysbiosis, fibrosis, and itch response. For this reason, agents selectively targeting IL-13, such as lebrikizumab, emerged as a potential therapy for AD. This article reviews the current evidence about lebrikizumab in the management of AD. The phase II and phase III trials seem to corroborate efficacy of lebrikizumab in the treatment of moderate-to-severe AD, as shown by significant improvement of Eczema Area and Severity Index, body surface area, and pruritus scores. Also, lebrikizumab demonstrated favorable safety and tolerability profiles, with the majority of patients experiencing no significant adverse events. Lebrikizumab seems to be a promising emerging targeted biological agent for patients with moderate-to-severe AD. More data on the long-term efficacy and safety, head-to-head comparisons with other agents, and real-world evidence will help to clarify its place in therapy in AD.
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Emollients and ceramide-based moisturizers restore lipid composition, reduce transepidermal water loss, and limit allergen and microbial penetration.
“Management includes both barrier repair options and targeted immunomodulation, with emollients and ceramide-based moisturizers, which restore lipid composition, reduce transepidermal water loss, and limit allergen and microbial penetration.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [12]
The Introduction identifies skin emollients as a mainstay of atopic dermatitis treatment. The section ‘The Role of Interleukin-13 in the Pathogenesis of AD’ says barrier damage increases transepidermal water loss and permits allergens and microorganisms to enter the skin. It does not say that emollients or ceramide-based moisturizers restore lipid composition or produce the claimed barrier effects; page numbers were not provided in our copy. (LLM, conf=0.83)
Experimental — accuracy not yet measuredThese atopic dermatitis therapies reduce inflammation and contribute to restoration of barrier function.
“These therapies reduce inflammation and contribute to the restoration of barrier function.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [12]
The Discussion (page unavailable) says IL-13 contributes to both inflammation and epidermal barrier disruption, and describes therapies that inhibit IL-13. It reports clinical improvement with lebrikizumab, but does not state that these therapies restore barrier function; that part is a plausible inference rather than a reported effect. (LLM, conf=0.82)
Experimental — accuracy not yet measuredTreatment of atopic dermatitis targets epidermal barrier dysfunction and type 2 immune dysregulation.
“Treatment of atopic dermatitis targets the epidermal barrier dysfunction and type 2 immune dysregulation.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [12]
In moderate-to-severe atopic dermatitis, systemic immunosuppressants such as cyclosporine, methotrexate, azathioprine, and mycophenolate mofetil can be used, alongside oral JAK inhibitors that interfere with intracellular signaling pathways central to disease pathogenesis.
“In moderate-to-severe disease, systemic immunosuppressants can be used, such as cyclosporine, methotrexate, azathioprine, and mycophenolate mofetil, alongside oral JAK inhibitors that interfere with intracellular signaling pathways central to disease pathogenesis.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [12]
Topical corticosteroids and calcineurin inhibitors remain first-line treatments for atopic dermatitis, while topical JAK inhibitors provide targeted inhibition of cytokine signaling downstream of IL-4 and IL-13.
“Topical anti-inflammatory therapies, including corticosteroids and calcineurin inhibitors, remain first-line treatments, while topical JAK inhibitors provide targeted inhibition of cytokine signaling downstream of IL-4 and IL-13.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [12]
Biologic therapies targeting type 2 inflammation, including dupilumab, lebrikizumab, and tralokinumab, have shown significant efficacy in moderate-to-severe atopic dermatitis by inhibiting IL-4 and IL-13 signaling.
“Biologic therapies targeting type 2 inflammation, including dupilumab, lebrikizumab, and tralokinumab, have shown significant efficacy in moderate-to-severe atopic dermatitis by inhibiting IL-4 and IL-13 signaling [11,12,13,14,15].”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [12]
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Tinca, A. C., Cozac-Szoke, A. R., & Cotoi, O. S. (2026) · Dermatopathology · doi:10.3390/dermatopathology13020022 · Cited by 1 · see citing works
- Authors
- Bernardo, D., Bieber, T., & Torres, T.
- Affiliations
- Hospital de Santo António (PT)
- University Hospital Bonn (DE)
- Universidade do Porto (PT)
- Corresponding author
- Torres, Tiago
- Venue
- American Journal of Clinical Dermatology
- Published
- 2023-06-02
- Volume
- 24
- Issue
- 5
- Pages
- 753-764
- ISSN
- 1175-0561 (ISSN-L)
- 1179-1888
- PMC
- PMC10460333
- OpenAlex
- W4379094582
- Cited by
- 43
- References
- 45
- Citations by year
- 2026: 8 · 2025: 25 · 2024: 9 · 2023: 1
- FWCI
- 1.96
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- American Journal of Clinical Dermatology (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- Universidade do Porto
- Topics
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- lebrikizumab, atopic dermatitis, IL-13, type 2 inflammation, pruritus, Eczema Area and Severity Index, skin barrier dysfunction, treatment efficacy and safety
- MeSH terms
- Antibodies, Monoclonal, Dermatitis, Atopic, Humans, Pruritus, Quality of Life, Severity of Illness Index, Treatment Outcome, Interleukin-13
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