Safety and Danger Considerations of Novel Treatments for Atopic Dermatitis in Context of Primary Cutaneous Lymphomas
Open accessAbstract
The impact of new and emerging therapies on the microenvironment of primary cutaneous lymphomas (PCLs) has been recently raised in the literature. Concomitantly, novel treatments are already used or registered (dupilumab, upadacitinib) and others seem to be added to the armamentarium against atopic dermatitis. Our aim was to review the literature on interleukins 4, 13, 22, and 31, and JAK/STAT pathways in PCLs to elucidate the safety of using biologics (dupilumab, tralokinumab, fezakinumab, nemolizumab) and small molecule inhibitors (upadacitinib, baricitinib, abrocitinib, ruxolitinib, tofacitinib) in the treatment of atopic dermatitis. We summarized the current state of knowledge on this topic based on the search of the PubMed database and related references published before 21 October 2021. Our analysis suggests that some of the mentioned agents (dupilumab, ruxolitinib) and others may have a direct impact on the progression of cutaneous lymphomas. This issue requires further study and meticulous monitoring of patients receiving these drugs to ensure their safety, especially in light of the FDA warning on tofacitinib. In conclusion, in the case of the rapid progression of atopic dermatitis/eczema, especially in patients older than 40 years old, there is a necessity to perform a biopsy followed by a very careful pathological examination.
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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 [18]
Section 2.1, “New Medications in AD” (page unavailable), describes nemolizumab targeting IL-31 signaling and acting on cutaneous sensory neurons, supporting neuroimmune pathway targeting. The passages found do not describe microbiome modulation or biomarker-guided treatment selection as emerging strategies for atopic dermatitis; searches for microbiome, microbial treatment, biomarkers, and patient selection did not establish those parts. (LLM, conf=0.86)
Experimental — accuracy not yet measuredRecent 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 [18]
Section 2.1, “New Medications in AD” (page unavailable), reports that JAK inhibitors were effective in phase III trials, including trials in moderate-to-severe atopic dermatitis. It does not report completed real-world effectiveness evidence or effectiveness specifically among patients who had responded inadequately to biologic therapies; the real-world upadacitinib study listed in the References was prospective. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThese IL-17-producing populations produce IL-17A, IL-17F, IL-22, TNF-α, and other mediators that act directly on keratinocytes.
“These populations produce IL-17A, IL-17F, IL-22, TNF-α, and other mediators that act directly on keratinocytes.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [18]
Section 2.3 (page unavailable) says Th22 lymphocytes and other immune subsets secrete IL-22, and reports IL-22 production by cultured CTCL cells. It does not establish that the specified populations produce the full list of IL-17A, IL-17F, IL-22 and TNF-α, or that those mediators act directly on keratinocytes; searches for those terms found no supporting passage. (LLM, conf=0.82)
Experimental — accuracy not yet measuredIL-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 [18]
Section 2.3 (page unavailable) links IL-22 activation to CCL20 activity and says enhanced CCL20 activity may induce epidermal hyperplasia. It does not state that IL-22 directly stimulates keratinocyte hyperplasia or abnormal differentiation, or describe acanthosis, parakeratosis, or loss of the granular layer. (LLM, conf=0.82)
Experimental — accuracy not yet measuredTNF-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 [18]
Section 2.3 (page unavailable) says IL-22 induces CCL20 and STAT3 expression in the context of cutaneous T-cell lymphoma. It does not address whether TNF-α, IL-17, and IL-22 magnify transcriptional responses in keratinocytes or endothelial cells; searches for those cell types and cytokine combinations found no such passage. (LLM, conf=0.74)
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 [18]
The Discussion (§2.3; page not provided) links IL-22 and CCL20 to epidermal hyperplasia and cell migration, but does not describe the claimed IL-17 response in keratinocytes. Searches for IL-17, keratinocytes, antimicrobial peptides, and leukocyte recruitment found no passage in our copy stating that mechanism. (LLM, conf=0.75)
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Dupilumab as a therapy option for treatment refractory mogamulizumab-associated rash
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Effectiveness of ustekinumab in patients with atopic dermatitis: analysis of real-world evidence
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IL-31 and IL-8 in Cutaneous T-Cell Lymphoma: Looking for Their Role in Itch
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Novel therapeutic approaches for cutaneous T cell lymphomas
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Self-citationClinical Guidelines and New Molecular Targets for Cutaneous Lymphomas
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Safety and danger of biologic treatments in psoriasis in context of cutaneous T-cell lymphoma (CTCL)
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Self-citationOlszewska, B., Żawrocki, A., Lakomy, J., Karczewska, J., Gleń, J., Zabłotna, M., Malek, M., Jankau, J. A., Lange, M., Biernat, W., et al. (2020) · International Journal of Dermatology · doi:10.1111/ijd.15036 · Cited by 4 · see citing works
Self-citationNihal, M., Wu, J., Stonesifer, C. J., Daniels, J., Choi, J., Geskin, L. J., Rook, A. H., & Wood, G. S. (2021) · Journal of Investigative Dermatology · doi:10.1016/j.jid.2021.06.034 · Cited by 4 · see citing works
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Research works printed but not linked: 1
- [32]NCT03568071—A Study to Assess Efficacy, Safety, Tolerability and Pharmacokinetics (PK)/Pharmacodynamics (PD) of MOR106 in Subjects with Moderate to Severe Atopic Dermatitis Available online: https://www.cochranelibrary.com/central/doi/10.1002/central/CN-01660617/full (accessed on 16 October 2021) · DOI
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Expert consensus on the systemic treatment of atopic dermatitis in special populations
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Dupilumab-Associated Lymphoid Reactions in Patients With Atopic Dermatitis
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How to Understand Personalized Medicine in Atopic Dermatitis Nowadays?
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Self-citationDevelopment of Cutaneous T-Cell Lymphoma Following Biologic Treatment: A Systematic Review
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Dupilumab, Atopic Dermatitis, and Mycosis Fungoides—New Insights on an Evolving Story
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Pharmacological Trends in the Management of Atopic Dermatitis: A Comprehensive Review
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Cutaneous T-cell lymphoma in a JAK inhibitor patient: A case report
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“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 [18–22].”
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Stark juckende Mycosis fungoides erfolgreich mit Upadacitinib behandelt
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Dupilumab-Associated Reversible Lymphoid Reaction Mimicking Mycosis Fungoides
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- Authors
- Kołkowski, K., Trzeciak, M., & Sokołowska-Wojdyło, M.
- Affiliations
- Gdańsk Medical University (PL)
- Department of Dermatology, Venereology and Allergology, Faculty of Medicine, Medical University of Gdansk, 80-214 Gdansk, Poland
- Corresponding author
- Kołkowski, Karol
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2021-12-13
- Volume
- 22
- Issue
- 24
- Pages
- 13388
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC8703592
- OpenAlex
- W4200609820
- Cited by
- 30
- References
- 190
- Citations by year
- 2026: 6 · 2025: 4 · 2024: 7 · 2023: 11 · 2022: 2
- FWCI
- 0.89
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Health Sciences › Medicine › Dermatology › Cutaneous lymphoproliferative disorders research
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Health Sciences › Medicine › Dermatology › Contact Dermatitis and Allergies
- Keywords
- atopic dermatitis, primary cutaneous lymphoma, dupilumab, upadacitinib, JAK/STAT inhibitors, IL-4, IL-13, IL-22, IL-31, biologic safety, ruxolitinib, tofacitinib, FDA warning
- MeSH terms
- Azetidines, Dermatitis, Atopic, Humans, Interleukins, Lymphoma, Nitriles, Piperidines, Purines, Pyrazoles, Pyrimidines, Skin Neoplasms, Sulfonamides, Signal Transduction, STAT Transcription Factors, Janus Kinases, Lymphoma, Primary Cutaneous Anaplastic Large Cell, Tumor Microenvironment, Antibodies, Monoclonal, Humanized
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