Peripheral itch sensitization in atopic dermatitis
Open accessAbstract
Atopic dermatitis is a skin disorder caused by skin dryness and barrier dysfunction, resulting in skin inflammation and chronic itch (or pruritus). The pathogenesis of atopic dermatitis is thought to be initiated by a lowering of the itch threshold due to dry skin. This lowering of the itch threshold is at least partially due to the increase in intraepidermal nerve fibers and sensitization of sensory nerves by interleukin (IL)-33 produced and secreted by keratinocytes. Such skin is easily prone to itch due to mechanical stimuli, such as rubbing of clothing and chemical stimuli from itch mediators. In patients with atopic dermatitis, once itch occurs, further itch is induced by scratching, and the associated scratching breaks down the skin barrier. Disruption of the skin barrier allows entry into the epidermis of external foreign substances, such as allergens derived from house dust mites, leading to an increased induction of type 2 inflammatory responses. As a result, type 2 cytokines IL-4, IL-13, and IL-31 are mainly secreted by Th2 cells, and their action on sensory nerve fibers causes further itch sensitization. These sequences of events are thought to occur simultaneously in patients with atopic dermatitis, leading to a vicious itch-scratch cycle. This vicious cycle becomes a negative spiral that leads to disease burden. Therefore, controlling itch is essential for the treatment of atopic dermatitis. In this review, we summarize and discuss advances in the mechanisms of peripheral itch sensitization in atopic dermatitis, focusing on skin barrier-neuro-immune triadic connectivity.
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The type 2 cytokine milieu downregulates antimicrobial peptides, facilitating microbial colonization, particularly by Staphylococcus aureus, which amplifies inflammation through superantigen production and Th2 polarization.
“Furthermore, this cytokine milieu downregulates antimicrobial peptides, facilitating microbial colonization, particularly by Staphylococcus aureus, which amplifies inflammation through superantigen production and Th2 polarization.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [9]
In “Itch mediators other than histamine” (page unavailable), the paper says that β-defensins, a class of antimicrobial peptides, are highly expressed in the epidermis of patients with atopic dermatitis—not that they are downregulated. It does not describe the claimed Staphylococcus aureus colonization, superantigen production, or Th2-polarization chain. (LLM, conf=0.78)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredEpithelial-derived alarmins such as TSLP, IL-25, and IL-33 activate dendritic cells and group 2 innate lymphoid cells (ILC2s), promoting Th2 differentiation and perpetuating cytokine release.
“In parallel, epithelial-derived alarmins such as TSLP, IL-25, and IL-33 activate dendritic cells and group 2 innate lymphoid cells (ILC2s), promoting Th2 differentiation and perpetuating cytokine release [7,8,9].”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [9]
The “Normal skin” section (page not available in our copy) says that keratinocyte-derived IL-33 and TSLP activate ILC2, which secrete IL-13 and IL-5 and induce type 2 inflammation. It does not establish the claimed role of IL-25, activation of dendritic cells by these alarmins, or the resulting Th2 differentiation. (LLM, conf=0.88)
Experimental — accuracy not yet measuredChronic atopic dermatitis is thought to be sustained by skin-resident memory T cells, which rapidly produce type 2 cytokines and contribute to recurrent inflammation.
“Chronic disease is thought to be sustained by skin-resident memory T cells, which rapidly produce type 2 cytokines and contribute to recurrent inflammation.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [9]
The “Normal skin” passage says Th2 cells secrete type 2 cytokines in acute atopic dermatitis lesions, and “Chronic lesion of atopic dermatitis” describes a continuing inflammatory response. Neither passage identifies those cells as skin-resident memory T cells or says they rapidly produce cytokines to drive recurrence. Page numbers are unavailable in our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measuredEosinophils, activated downstream of IL-5 and type 2 cytokines, contribute to tissue remodeling and inflammation.
“Eosinophils, activated downstream of IL-5 and type 2 cytokines, further contribute to tissue remodeling and inflammation.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [9]
The IL-33 section (page unavailable) says IL-33 activates eosinophils involved in allergic inflammation. The Normal skin section (page unavailable) says ILC2 secrete IL-5 and IL-13 to induce type 2 inflammation. Neither passage says IL-5 activates eosinophils or that eosinophils contribute to tissue remodeling. (LLM, conf=0.82)
Experimental — accuracy not yet measuredIL-4, IL-13, and IL-31, produced upon antigen re-exposure, maintain inflammation even in clinically normal skin.
“IL-4, IL-13, and IL-31, produced upon antigen re-exposure, maintain inflammation even in clinically normal skin.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [9]
The “Normal skin” section says allergen antigens can trigger a type 2 inflammatory response, but places IL-4, IL-13, and IL-31 secretion in acute atopic dermatitis lesions. It does not say these three cytokines are produced upon antigen re-exposure or maintain inflammation in clinically normal skin; it describes the immune response in normal skin as normal. Page numbers are unavailable in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measured
Type 2 inflammatory cytokines IL-4 and IL-13 signal through JAK-dependent pathways and lead to activation of STAT6.
“Type 2 inflammatory cytokines, IL-4 and IL-13, signal through JAK-dependent pathways and lead to activation of STAT6.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [9]
The “Type 2 cytokines: IL-4 and IL-13” section identifies both as type 2 cytokines and says JAK1 is responsible for intracellular IL-4 receptor signaling. It does not state that both cytokines activate STAT6, so the full signaling pathway attributed to the paper is not supported by our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredAtopic dermatitis is driven by a complex interaction between epidermal barrier defects and immune dysregulation, with the IL-4/IL-13-JAK-STAT6 axis representing a central pathogenic pathway.
“Atopic dermatitis is driven by a complex interaction between epidermal barrier defects and immune dysregulation, with the IL-4/IL-13–JAK–STAT6 axis representing a central pathogenic pathway.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [9]
The Abstract (page unavailable) describes barrier dysfunction leading to inflammation and type 2 immune responses, supporting the interaction between barrier defects and immune activity. The “Type 2 cytokines: IL-4 and IL-13” section links those cytokines to itch sensitization and tentatively implicates JAK1, but does not identify a JAK–STAT6 axis as a central pathogenic pathway. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn atopic dermatitis, barrier dysfunction and type 2 immune responses reciprocally reinforce each other in a self-amplifying loop that underlies disease initiation and chronicity.
“Collectively, these mechanisms establish a self-amplifying loop in which barrier dysfunction and type 2 immune responses reciprocally reinforce each other, underlying both disease initiation and chronicity in atopic dermatitis [9,10].”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [9]
IL-4 and IL-13 directly sensitize sensory neurons and enhance pruritogenic signaling.
“Additionally, neuroimmune interactions also contribute, as IL-4 and IL-13 directly sensitize sensory neurons and enhance pruritogenic signaling.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [9]
IL-4/IL-13-JAK-STAT6 signaling results in transcriptional repression of epidermal differentiation genes such as filaggrin, loricrin, and involucrin, and enzymes involved in ceramide synthesis, thereby impairing barrier integrity.
“This results in transcriptional repression of essential epidermal differentiation genes such as filaggrin, loricrin, and involucrin, as well as enzymes involved in ceramide synthesis, thereby directly impairing barrier integrity.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [9]
The “Type 2 cytokines: IL-4 and IL-13” section discusses IL-4/IL-13 signaling and JAK1 in sensory-nerve itch sensitization, not repression of epidermal genes. Searches for filaggrin, loricrin, involucrin, ceramide synthesis, and STAT6 found no passage in our copy addressing the claimed gene repression or its effect on barrier integrity. (LLM, conf=0.75)
Experimental — accuracy not yet measured
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Flagged first, then by citations
Research works printed but not linked: 3
- St€ ander S, Grundmann SA. Chronic pruritus. G Ital Dermatol Venereol 2012;147:161e9.
- Wilzopolski J, Kietzmann M, Mishra SK, Stark H, Baumer W, Rossbach K. TRPV1 and TRPA1 channels are both involved downstream of histamine- induced itch. Biomolecules 2021;11:1166.
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Cited by
Sorted by citations
Neuroimmune mechanisms of type 2 inflammation in the skin and lung
Tamari, M., & Ver Heul, A. M. (2025) · Allergology International · doi:10.1016/j.alit.2025.02.001 · Cited by 17 · see citing works
Tinca, A. C., Cozac-Szoke, A. R., & Cotoi, O. S. (2026) · Dermatopathology · doi:10.3390/dermatopathology13020022 · Cited by 1 · see citing works
“Collectively, these mechanisms establish a self-amplifying loop in which barrier dysfunction and type 2 immune responses reciprocally reinforce each other, underlying both disease initiation and chronicity in atopic dermatitis [9,10].”
- Authors
- Tominaga, M., & Takamori, K.
- Affiliations
- Juntendo University (JP)
- Corresponding author
- Tominaga, Mitsutoshi
- Venue
- Allergology International
- Publisher
- Elsevier BV
- Published
- 2022-07
- Volume
- 71
- Issue
- 3
- Pages
- 265-277
- ISSN
- 1323-8930 (ISSN-L)
- OpenAlex
- W4281485602
- Cited by
- 160
- References
- 137
- Citations by year
- 2026: 38 · 2025: 56 · 2024: 32 · 2023: 28 · 2022: 6
- FWCI
- 5.43
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Allergology International (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Cosmetology Research Foundation
- Japan Society for the Promotion of Science (22H02956, 23K20320, S1311011, 18K07396, 20H03568, 23K24217)
- Topics
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Health Sciences › Medicine › Dermatology › Contact Dermatitis and Allergies
- Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
- Keywords
- atopic dermatitis, pruritus, itch-scratch cycle, skin barrier dysfunction, IL-33, keratinocytes, intraepidermal nerve fibers, type 2 cytokines, IL-4, IL-13, IL-31, Th2 cells, house dust mite allergens, neuroimmune interactions
- MeSH terms
- Allergens, Dermatitis, Atopic, Epidermis, Humans, Pruritus, Skin, Cytokines
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