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Contact Dermatitis

Asta Literature Retrieval: Contact Dermatitis pathophysiology mechanisms phenotypes

2026-03-13
Asta MONDO:0005480 Model: Asta Scientific Corpus Retrieval 65 citations

Asta Literature Retrieval: Contact Dermatitis pathophysiology mechanisms phenotypes

This report is retrieval-only and is generated directly from Asta results.

  • Papers retrieved: 65
  • Snippets retrieved: 20

Relevant Papers

[1] Allergic contact dermatitis: pathophysiology applied to future therapy

  • Authors: Lily Li, P. Cruz
  • Year: 2004
  • Venue: Dermatologic Therapy
  • URL: https://www.semanticscholar.org/paper/22049b3a38538ebb26c3d0f96425fa4d5b63f5b8
  • DOI: 10.1111/j.1396-0296.2004.04023.x
  • PMID: 15186367
  • Citations: 34
  • Influential citations: 1
  • Summary: The pathogenesis and current treatment of allergic contact dermatitis and speculates on the prospects for improved future therapy are reviewed.
  • Evidence snippets:
  • Snippet 1 (score: 0.534) > Allergic contact dermatitis: pathophysiology applied to future therapy
  • Snippet 2 (score: 0.508) > ABSTRACT:  Contact dermatitis is a common reason for patient visits to primary‐care clinics and represents up to 7% of all dermatologic consultations in the US. Substantial progress has been made in elucidating the pathophysiology of contact dermatitis, particularly the allergic form. A better understanding of pathologic mechanisms has led to improved management of cases and will continue to advance treatment modalities. The present paper reviews the pathogenesis and current treatment of allergic contact dermatitis and speculates on the prospects for improved future therapy.

[2] Coexistence of Allergic Contact Dermatitis and Immediate-Type Hypersensitivity Reactions, Two Contrasting Immunological Responses: A Literature Review

[3] CD100 boosts the inflammatory response in the challenge phase of allergic contact dermatitis in mice

[4] miRNAs’ Cross-Involvement in Skin Allergies: A New Horizon for the Pathogenesis, Diagnosis and Therapy of Atopic Dermatitis, Allergic Contact Dermatitis and Chronic Spontaneous Urticaria

[5] Tissue-Resident Trouble: How TRM Cells Drive Allergic Contact Dermatitis

[6] IL22RA2 is a Smad7 target mediating alleviation of dermatitis and psoriatic phenotypes in mice.

[7] Recent Developments and Advances in Atopic Dermatitis: A Focus on Epidemiology, Pathophysiology, and Treatment in the Pediatric Setting

  • Authors: L. Eichenfield, Stephen Stripling, Selwyn Fung, A. Cha, Andryann O’Brien et al.
  • Year: 2022
  • Venue: Paediatric Drugs
  • URL: https://www.semanticscholar.org/paper/aff13e2dcb3dccbf496f436dd93f3bf898215377
  • DOI: 10.1007/s40272-022-00499-x
  • PMID: 35698002
  • PMCID: 9191759
  • Citations: 80
  • Influential citations: 5
  • Summary: Recent advances in scientific research regarding the mechanisms involved in the pathogenesis of atopic dermatitis that have resulted in the discovery of novel therapeutic targets and the development of targeted biologic therapies with the potential to revolutionize AD therapy are highlighted.

[8] Eyelid Contact Dermatitis: 25-Year Single-Center Retrospective Study

  • Authors: G. Rubegni, Tommaso Padula, L. Calabrese, M. D’Onghia, L. Tognetti et al.
  • Year: 2025
  • Venue: Journal of Clinical Medicine
  • URL: https://www.semanticscholar.org/paper/58ddf9aaebf7e17e684028a21a25b94147f5ac43
  • DOI: 10.3390/jcm14030823
  • PMID: 39941494
  • PMCID: 11818699
  • Citations: 3
  • Influential citations: 1
  • Summary: The haptens identified in eyelid ACD largely overlap with those found in other body regions, including metals, fragrances, and preservatives, however, the unique characteristics of eyelid skin and hand–eye contact patterns play a significant role in sensitization.

[9] Tolerogenic phenotype of dendritic cells is induced after hapten sensitization followed by attenuated contact hypersensitivity response in atopic dermatitis model NC/Nga mice.

  • Authors: Kanako Nakayama, Hiroe Tetsu, Taku Nishijo, T. Yuki, Masaaki Miyazawa
  • Year: 2023
  • Venue: Biochemical and biophysical research communications
  • URL: https://www.semanticscholar.org/paper/84f61913e47b4dff53340c5de76caf11475c2196
  • DOI: 10.1016/j.bbrc.2023.08.042
  • PMID: 37611349
  • Summary: Allergic contact dermatitis (ACD) and atopic dermatitis (AD) are common inflammatory diseases. We previously reported attenuated contact hypersensitivity (CHS) responses in AD model mice using 2,4-dinitrofluorobenzene, reflecting clinical experiments. However, previous studies have not addressed the commonality of findings across haptens and mechanisms focused on dendritic cells (DCs). Thus, this study evaluated CHS responses to fluorescein isothiocyanate (FITC) and DC migration and maturatio...

[10] Defining cell type-specific immune responses in a mouse model of allergic contact dermatitis by single-cell transcriptomics

[11] Atopic dermatitis phenotypes and the need for personalized medicine

[12] Addressing Unmet Needs in Atopic Dermatitis: Evaluating Disease-Modifying Capabilities of Current and Emerging Therapies

[13] Annexin 1 Reduces Dermatitis-Induced Itch and Cholestatic Itch through Inhibiting Neuroinflammation and Iron Overload in the Spinal Dorsal Horn of Mice

[14] Effector and regulatory mechanisms in allergic contact dermatitis

[15] Contact dermatitis I. Pathophysiology of contact sensitivity.

  • Authors: M. Krasteva, J. Kehren, M. Ducluzeau, M. Sayag, Marco Cacciapuoti et al.
  • Year: 1999
  • Venue: European journal of dermatology : EJD
  • URL: https://www.semanticscholar.org/paper/1949151c9f02e44825a44f440f5b96745e76a7b7
  • PMID: 9920992
  • Citations: 87
  • Influential citations: 3
  • Summary: Allergic contact dermatitis is one of the most common skin diseases, with a great socio-economic impact and according to the pathophysiological mechanisms involved, two main types of CD may be distinguished: allergicContact dermatitis (ACD) and irritant contact dermatritis (ICD).

[16] Integrated Mechanisms of Cutaneous Immunity: From Barrier Dysfunction to Neuroimmune Crosstalk in Inflammatory Skin Disease

  • Authors: Andrés Felipe, Herrera Homez, Hillary Yahiry, Mejía Montiel, María Camila et al.
  • Year: 2025
  • Venue: IECCMEXICO
  • URL: https://www.semanticscholar.org/paper/ec5216fb1359be98869809c9552584fae7a688b6
  • DOI: 10.64784/064
  • Summary: This review synthesizes contemporary evidence on epidermal barrier dysfunction, microbiome dysbiosis, antigen-presenting cell networks, tissue-resident memory T cells, and neuroimmune signaling to construct a comprehensive model explaining the pathophysiology of major inflammatory dermatoses, including atopic dermatitis, psoriasis, and allergic contact dermatitis.

[17] Proteome Profile of Trigeminal Ganglion in Murine Model of Allergic Contact Dermatitis: Complement 3 Pathway Contributes to Itch and Pain Sensation

[18] Pathophysiologic Mechanisms and Targeted Treatments Associated with the Nervous System in Cutaneous Allergic Diseases

[19] Biocompatibility and Post-Marketing Surveillance Study of Emollient Plus Medical Device Cream Containing Oligofructans from Ophiopogon japonicus and Acetyl Heptapeptide-4 in Atopic Dermatitis Skin Care

[20] Atopic Dermatitis and Allergic Contact Dermatitis in Pregnancy

[21] Atopic dermatitis: an expanding therapeutic pipeline for a complex disease

[22] Investigation of the underlying mechanisms leading to the development of incontinence-associated dermatitis.

[23] Ghrelin protects against contact dermatitis and psoriasiform skin inflammation by antagonizing TNF-α/NF-κB signaling pathways

[24] Melasma: Pathophysiology, Clinical Picture and Treatment Lines Overview

[25] Exploring the pathophysiological mechanisms and wet biomarkers of VPS13A disease

[26] Euphorbia myrsinites Sap-Induced Phytodermatitis: A Prototype of Irritant Contact Dermatitis?

[27] 014 IL-27 induces IL-15 production to facilitate T cell survival in allergic contact dermatitis

[28] Allergic contact dermatitis due to neem oil: A case report and mini‐review

[29] When Foods Cause Itch: Clinical Characteristics, Pathophysiology, and Recommendations for Food-Induced Skin and Mucosal Pruritus

[30] THE ROLE OF KERATINOCYTES IN THE PATHOPHYSIOLOGY OF CONTACT DERMATITIS

[31] Perspectives in the Molecular Mechanisms Underlying Anaphylaxis.

[32] The mystery of methylmercury-perturbed calcium homeostasis: AMPK-DRP1-dependent mitochondrial fission initiates ER-mitochondria contact formation.

[33] Mechanisms of contact sensitization offer insights into the role of barrier defects versus intrinsic immune abnormalities as drivers of atopic dermatitis

  • Authors: N. Dhingra, Nicholas Gulati, E. Guttman‐Yassky
  • Year: 2013
  • Venue: The Journal of investigative dermatology
  • URL: https://www.semanticscholar.org/paper/7e6041bef9a50ab503d4768e54901a8ea6288acb
  • DOI: 10.1038/jid.2013.239
  • PMID: 24030647
  • PMCID: 3773606
  • Citations: 39
  • Influential citations: 1
  • Summary: In this issue, Newell et al. (2013) used an experimental contact sensitization model with dinitrochlorobenzene (DNCB) to gain insight into the unique immune phenotype of AD patients.
  • Evidence snippets:
  • Snippet 1 (score: 0.410) > Atopic dermatitis (AD) is a common inflammatory skin disease characterized by wet, oozing, erythematous, pruritic lesions in the acute stage and xerotic, lichenified plaques in the chronic stage. It frequently coexists with asthma and allergic rhinitis, sharing some mechanistic features with these diseases as part of the "atopic march." Controversy exists as to whether immune abnormalities, epidermal barrier defects, or both are the primary factors responsible for disease pathogenesis. In AD patients, there is often a coexisting irritant contact dermatitis (ICD) or allergic contact dermatitis (ACD) that is sometimes clinically difficult to distinguish from AD. ACD shares molecular mechanisms with AD, including increased cellular infiltrates and cytokine activation (Gittler et al., 2013). In this issue, Newell et al. (2013) used an experimental contact sensitization model with dinitrochlorobenzene (DNCB) to gain insight into the unique immune phenotype of AD patients.

[34] Atopic dermatitis endotypes: knowledge for personalized medicine

[35] Recent Advancements in the Atopic Dermatitis Mechanism.

[36] Atopic dermatitis: a brief review of recent advances in management

[37] Advances in Current Drugs and Formulations for the Management of Atopic Dermatitis.

[38] When Foods Cause Itch: Clinical Characteristics, Pathophysiology, and Recommendations for Food-Induced Skin and Mucosal Pruritus.

[39] 1605a Individual susceptibility to work-related contact dermatitis

[40] Effects of chloromethylisothiazolinone/methylisothiazolinone (CMIT/MIT) on Th2/Th17-related immune modulation in an atopic dermatitis mouse model

[41] Intrinsic Atopic Dermatitis and Extrinsic Atopic Dermatitis: Similarities and Differences

[42] Irritant contact dermatitis

[43] Allergic Contact Dermatitis in Psoriasis Patients: Typical, Delayed, and Non-Interacting

[44] Atopic dermatitis: an expanding therapeutic pipeline for a complex disease

[45] Models of contact dermatitis and atopic eczema

[46] Multiple Roles for Cytokines in Atopic Dermatitis: From Pathogenic Mediators to Endotype-Specific Biomarkers to Therapeutic Targets

[47] Microbial–Host Interactions in Dermatologic Inflammation: Ecological, Immunological, and Clinical Perspectives

  • Authors: Carolina Paola Ortiz Valdés, Xóchitl Monteon Aspeitia, Hillary Yahiry Mejía Montiel, Silvana Cabrera Puentes, Claudia Zamaly Ferreira Hernández et al.
  • Year: 2025
  • Venue: International Science Journal
  • URL: https://www.semanticscholar.org/paper/5d064bf684e9703b09ce04e03ff0fba20390b880
  • DOI: 10.64784/050
  • Summary: The evidence underscores the microbiome’s central role in shaping cutaneous inflammation and emphasizes the need for geographically inclusive research and translational innovation to support future dermatologic practice.

[48] Itch in Chronic Wounds: Pathophysiology, Impact, and Management

[49] New Potential of Roxatidine Acetate Hydrochloride on Atopic Dermatitis Mouse Model, Human Keratinocytes, and Human Skin Equivalent Model

[50] Sebaceous immunobiology - skin homeostasis, pathophysiology, coordination of innate immunity and inflammatory response and disease associations

  • Authors: C. Zouboulis, T. Coenye, Li He, K. Kabashima, Tetsuro Kobayashi et al.
  • Year: 2022
  • Venue: Frontiers in Immunology
  • URL: https://www.semanticscholar.org/paper/b67f52b6d6626f4c279a260ee58e0dd81ebad203
  • DOI: 10.3389/fimmu.2022.1029818
  • PMID: 36439142
  • PMCID: 9686445
  • Citations: 94
  • Influential citations: 2
  • Summary: This review presents several aspects of the innovative concept of sebaceous immunobiology, which summarizes the numerous activities of the sebaceous gland including its classical physiological and pathophysiological tasks, namely sebum production and the development of seborrhea and acne. Sebaceous lipids, which represent 90% of the skin surface lipids in adolescents and adults, are markedly involved in the skin barrier function and perifollicular and dermal innate immune processes, leading t...

[51] Advancing the understanding of allergic contact dermatitis: from pathophysiology to novel therapeutic approaches

  • Authors: M. Tramontana, K. Hansel, L. Bianchi, Chiara Sensini, N. Malatesta et al.
  • Year: 2023
  • Venue: Frontiers in Medicine
  • URL: https://www.semanticscholar.org/paper/1edb98767206171ef69fe0a0df8629b66fb6d56f
  • DOI: 10.3389/fmed.2023.1184289
  • PMID: 37283623
  • PMCID: 10239928
  • Citations: 61
  • Influential citations: 2
  • Summary: Patch testing with suspected allergens is required for a diagnosis of allergic contact dermatitis and metals, especially nickel, fragrance mix, isothiazolinones, and para-phenylenediamine are the most commonly positive allergens in patients patch tested for suspected ACD.
  • Evidence snippets:
  • Snippet 1 (score: 0.575) > Advancing the understanding of allergic contact dermatitis: from pathophysiology to novel therapeutic approaches

[52] Para-Phenylenediamine Sensitization and Polysensitization: TNF-α, CXCL11, and Immune-Regulatory Gene Polymorphisms

  • Authors: Jin Ju Lee, Heera Lee, J. Byun, You Won Choi, J. Roh et al.
  • Year: 2025
  • Venue: Annals of Dermatology
  • URL: https://www.semanticscholar.org/paper/74350d9355d45033fb25fe457a4f8a17f9ab619a
  • DOI: 10.5021/ad.25.102
  • PMID: 41044808
  • PMCID: 12505369
  • Summary: PPD sensitization identifies patients at increased risk for PS and reactivity to mercury compounds and fragrance-related substances and preliminary genetic observations require validation in larger studies to determine potential immunogenetic contributions.
  • Evidence snippets:
  • Snippet 1 (score: 0.502) > Despite genetic analysis limitations, our study advances the understanding of contact allergy pathophysiology by demonstrating that PPD sensitization and PS represent distinct but overlapping immunological phenotypes with characteristic correlation signatures. While preliminary genetic observations require validation in larger studies, the clinical findings regarding PPD-mercury and PPD-fragrance associations, along with the comprehensive PS patterns, provide actionable insights for patch testing strategies and patient counseling.
  • Snippet 2 (score: 0.425) > From the full cohort, a subset of 17 individuals was selected for exploratory genetic analysis using convenience sampling to represent 4 distinct phenotypic groups: (1) PPD+/PS+ (n=7), (2) PPD+/ PS− (n=2), (3) PPD−/PS+ (n=6), and (4) PPD−/PS− (n=2). > Peripheral blood samples were collected for DNA extraction. Five SNPs were selected based on their established roles in contact dermatitis pathophysiology and immune regulation: TNF-α (rs1800629) encodes a key pro-inflammatory cytokine regulating keratinocyte activation and inflammatory responses in ACD 9 ; CXCL11 (rs6817952) encodes an interferon-inducible chemokine crucial for T-cell recruitment and trafficking to allergen exposure sites 13 ; IL-10 (rs1800871) encodes an anti-inflammatory cytokine essential for immune tolerance and inflammation regulation 11 ; IL-16 (rs4778889) encodes a CD4+ T-cell chemoattractant and PPD Sensitization and Polysensitization https://anndermatol.org key mediator in delayed-type hypersensitivity reactions 12 ; and STAT6 (rs1059513) encodes a transcription factor critical for Th2 cell differentiation and allergic immune responses 10 . These polymorphisms represent key nodes in immune pathways relevant to contact sensitization susceptibility. > Statistical analyses were conducted using SPSS version 25.0 (IBM Corp., Armonk, NY, USA) and R version 4.0.3 (R Foundation for Statistical Computing, Vienna, Austria). Intergroup comparisons utilized χ 2 or Fisher's exact test for categorical data, and t-tests or Mann-Whitney U tests for continuous data. Binary logistic regression was performed to evaluate associations between clinical factors and sensitization status, adjusting for potential confounders. For genetic analyses, Fisher's exact test compared genotype frequencies between phenotypic subgroups, with p-values≤0.05 considered statistically significant.
  • Snippet 3 (score: 0.424) > Similarly, the exclusive detection of TNF-α variants in PPD-sensitized patients, while potentially interesting, is based on only 3 patients across all PPD-positive groups and cannot support meaningful conclusions about genetic associations 22,23 . The observed distribution patterns for IL-10, STAT6, and IL-16 polymorphisms across different sensitization phenotypes, though suggestive of potential involvement in immune regulation pathways 24,25 , are similarly limited by small sample sizes and require validation in larger cohorts. Given these limitations, we refrain from detailed mechanistic interpretations of individual polymorphisms and emphasize that our genetic findings represent preliminary observations that may guide future hypothesis-driven research rather than established associations. Nevertheless, the selected polymorphisms represent key nodes in immune pathways relevant to contact dermatitis pathogenesis, and the observed distribution patterns, though requiring validation in larger cohorts, align with the biological functions of these genes in orchestrating immune responses to contact allergens. > Several limitations must be acknowledged. First, the retrospective design and single-center nature of this study may limit the generalizability of findings to other populations with different allergen exposure patterns and genetic backgrounds. Second, the small number of patients who underwent SNP analysis (n=17) significantly limits the generalizability and statistical power of the genetic findings, preventing meaningful statistical comparisons and limiting conclusions about genetic associations. Third, our genetic analysis was limited to 5 selected polymorphisms and may not capture the full spectrum of genetic variants influencing contact sensitization. Fourth, the cross-sectional design prevents assessment of temporal relationships and causality between genetic factors and sensitization development. Fifth, the absence of population-matched genetic controls further limits interpretation of variant frequencies. Finally, longitudinal studies tracking sensitization patterns over time are warranted to determine whether correlation networks evolve or remain stable. Future larger-scale, multi-center studies with comprehensive immunogenetic profiling are essential to validate genetic associations. Adequately powered genetic with population-matched controls are needed to determine whether genetic variants in immune-regulatory pathways contribute to contact sensitization patterns. > Despite genetic analysis limitations, our study advances the understanding of contact allergy pathophysiology by demonstrating that PPD sensitization and PS represent distinct but overlapping immunological phenotypes with characteristic correlation signatures.

[53] Differential diagnosis of contact dermatitis: A practical‐approach review by the EADV Task Force on contact dermatitis

  • Authors: D. Pesqué, O. Aerts, M. Bizjak, M. Gonçalo, Aleksandra Dugonik et al.
  • Year: 2024
  • Venue: Journal of the European Academy of Dermatology and Venereology
  • URL: https://www.semanticscholar.org/paper/1a9753ec7f18a38c01e7a6c3df230cad141a8dc5
  • DOI: 10.1111/jdv.20052
  • PMID: 38713001
  • Citations: 23
  • Influential citations: 1
  • Summary: The Task Force aims to conduct a review of the unifying clinical features of contact dermatitis and characterize its main clinical phenotypes, and its simulators, in order to contribute to an early suspicion or recognition of contact dermatitis and enable a correct differential diagnosis.
  • Evidence snippets:
  • Snippet 1 (score: 0.489) > The diagnosis of eczema (‘dermatitis’) is mostly clinical and depends on the clinical history and exploratory objective findings (primary lesions, patterns). Contact dermatitis remains as an important condition in the group of eczematous disorders, with important socioeconomic and occupational relevance. Although irritant and allergic contact dermatitis have a different pathogenesis, both are characterized by a rather typical morphology, are triggered by external factors and tend to occur primarily in the area of contact with the exogenous agent. In addition, allergic and irritant dermatitis may also co‐exist. The importance of diagnosing contact dermatitis, especially when allergic in nature, is both due to the possibility of avoiding the trigger, and due to its role in aggravating other skin conditions. Nevertheless, the heterogeneity of clinical presentations in daily practice may pose an important challenge for the suspicion and correct diagnosis of contact dermatitis. Furthermore, other conditions, with different pathogenesis and treatment, may clinically simulate contact dermatitis. The Task Force aims to conduct a review of the unifying clinical features of contact dermatitis and characterize its main clinical phenotypes, and its simulators, in order to contribute to an early suspicion or recognition of contact dermatitis and enable a correct differential diagnosis.

[54] Contact dermatitis - Pathomechanism and understanding of disease in clinical setting

[55] Acetylation Phenotype Variation in Patients with Allergic Contact Dermatitis

[56] Emerging Links between Microbiome Composition and Skin Immunology in Diaper Dermatitis: A Narrative Review

  • Authors: Tjaša Hertiš Petek, Maya Petek, Tadej Petek, Nataša Marčun Varda
  • Year: 2022
  • Venue: Children
  • URL: https://www.semanticscholar.org/paper/d138abc5a7c67dd84e1e6a63bdab3d0c58cf7140
  • DOI: 10.3390/children9010112
  • PMID: 35053737
  • PMCID: 8775025
  • Citations: 17
  • Influential citations: 1
  • Summary: There is preliminary evidence that certain probiotics given orally or topically could be used as a gentle intervention in diaper dermatitis, suggesting introduction of probiotics is an attractive treatment for microbiome modulation.
  • Evidence snippets:
  • Snippet 1 (score: 0.444) > These results suggest that polymorphisms of individual nucleotides, associated with skin inflammation and homeostasis, can affect responses to irritants and at least partially explain individual differences in the development of contact dermatitis. IL-1α, IL-8 and TNF-α seem to be the most important cytokines in DD [8][9][10][11]42]. Inflammatory processes depend not only on the trigger but also on genetic predispositions [34,35]. However, the exact cytokine profile in DD is still unknown and likely varies between patients, the microbiome composition and the irritant nature.

[57] Cytokines and Chemokines in Irritant Contact Dermatitis

  • Authors: H. Lee, M. Stieger, N. Yawalkar, M. Kakeda
  • Year: 2013
  • Venue: Mediators of Inflammation
  • URL: https://www.semanticscholar.org/paper/5c186b8e8487b573aee2f7e52660a2fbe1d94247
  • DOI: 10.1155/2013/916497
  • PMID: 24371376
  • PMCID: 3858878
  • Citations: 127
  • Influential citations: 8
  • Summary: This review will focus on key cytokines and chemokines involved in the pathogenesis of irritant contact dermatitis and also contrast the differences between allergic contact dermatitus and irritantContact dermatitis.
  • Evidence snippets:
  • Snippet 1 (score: 0.436) > Irritant contact dermatitis (ICD) is an inflammatory response of the skin to various external stimuli. It arises as a result of activated innate immunity to direct injury of the skin without prior sensitization [1][2][3]. ICD is a complex reaction modulated by both intrinsic and extrinsic factors [2][3][4]. Intrinsic factors which influence the susceptibility to ICD include genetic predisposition, for example, atopic diathesis, age, sex, and body region. Extrinsic factors include the inherent nature of the irritants, exposure volume, concentration, duration, repetition, and the presence of further environmental and mechanical factors. > ICD has a spectrum of clinical features which can be divided into several different categories depending on the irritant and its exposure pattern. Ten clinical subtypes have been proposed [2]. The influence of irritants on various cytokines/chemokines has not been well delineated so far, although it is plausible that different environmental insults and the subsequent variation in cytokines/chemokines expression could result in distinct clinical phenotypes. > In this review, we discuss the pathophysiological mechanisms involved in ICD with a focus on key cytokines and chemokines as well as their cellular source in the skin. Furthermore, we highlight the key differences between ICD and allergic contact dermatitis (ACD).

[58] Differential susceptibility between skin and vaginal mucosa in sensitization phase of allergic contact dermatitis in mice

  • Authors: Taku Nishijo, Kanako Nakayama, M. Miyazawa, Y. Kuroda, H. Sakaguchi
  • Year: 2020
  • Venue: Immunity, Inflammation and Disease
  • URL: https://www.semanticscholar.org/paper/06bf6560caf60bd3baabc3a3daf4e299ca3d5d4e
  • DOI: 10.1002/iid3.351
  • PMID: 32914939
  • PMCID: 7654400
  • Citations: 3
  • Summary: Mechanisms underlying skin sensitization in allergic contact dermatitis have been actively studied using the murine contact hypersensitivity (CHS) model, but much less is known about sensitization at the vaginal mucosa.
  • Evidence snippets:
  • Snippet 1 (score: 0.433) > Mechanisms underlying skin sensitization in allergic contact dermatitis have been actively studied using the murine contact hypersensitivity (CHS) model. However, much less is known about sensitization at the vaginal mucosa (VM).

[59] Intricate Relationship Between Adaptive and Innate Immune System in Allergic Contact Dermatitis

  • Authors: M. Azeem, H. Kader, A. Kerstan, H. Hetta, E. Serfling et al.
  • Year: 2020
  • Venue: The Yale Journal of Biology and Medicine
  • URL: https://www.semanticscholar.org/paper/34345717c1dda542d64d9496d28fc675fdb24225
  • PMID: 33380932
  • PMCID: 7757059
  • Citations: 18
  • Influential citations: 1
  • Summary: The main cell types from both immune domains, which are involved in ACD, are focused on, such as CD4+ and CD8+ T cells, B cells, neutrophils, and innate lymphoid cells (ILCs), which can be useful for devising future therapeutic interventions for ACD.
  • Evidence snippets:
  • Snippet 1 (score: 0.412) > Allergic contact dermatitis (ACD) is a complex immunological allergic disease characterized by the interplay between the innate and adaptive immune system. Initially, the role of the innate immune system was believed to be confined to the initial sensitization phase, while adaptive immune reactions were linked with the advanced elicitation phase. However, recent data predicted a comparatively mixed and interdependent role of both immune systems throughout the disease progression. Therefore, the actual mechanisms of disease progression are more complex and interlinked. The aim of this review is to combine such findings that enhanced our understanding of the pathomechanisms of ACD. Here, we focused on the main cell types from both immune domains, which are involved in ACD, such as CD4+ and CD8+ T cells, B cells, neutrophils, and innate lymphoid cells (ILCs). Such insights can be useful for devising future therapeutic interventions for ACD.

[60] MUTZ-3 derived Langerhans cells in human skin equivalents show differential migration and phenotypic plasticity after allergen or irritant exposure.

  • Authors: I. Kosten, S. Spiekstra, T. D. de Gruijl, S. Gibbs
  • Year: 2015
  • Venue: Toxicology and applied pharmacology
  • URL: https://www.semanticscholar.org/paper/016c282bbcebc23731ea72bf3c21de657a8e8ed8
  • DOI: 10.1016/j.taap.2015.05.017
  • PMID: 26028481
  • Citations: 74
  • Influential citations: 2
  • Summary: Mechanisms previously identified as being involved in LC activation and migration in native human skin could thus be reproduced in the in vitro constructed skin equivalent model containing functional LC and will provide a powerful tool for hazard identification, testing novel therapeutics and identifying new drug targets.
  • Evidence snippets:
  • Snippet 1 (score: 0.411) > In this study we provide novel and further evidence that the MUTZ-3 cell line is the most physiologically relevant LC-like cell line identified to date since it shows a unique in vivo like plasticity upon exposure to environmental stimuli (e.g. allergens, irritants). In the past we showed that MUTZ-3 were able to differentiate in a cytokine dependent manner into Langerin expressing LC or, indeed, DC-SIGN expressing dermal DC (Masterson et al., 2002;van de Ven et al., 2011b), which are both able to prime specific T cell responses (Santegoets et al., 2006;Santegoets et al., 2008). Here we show that upon topical allergen exposure epidermal MUTZ-LC mature and migrate in a CXCL12 dependent, and CCL5 independent, manner to the dermal compartment of SE, whereas after topical irritant exposure they migrate in a CCL5 dependent, and CXCL12 independent, manner and undergo an IL-10 dependent phenotypic change to a macrophage-like cell within the dermal compartment. > The SE-LC was designed to enable complex mechanisms concerning human DC biology to be investigated in an animal alternative, physiologically relevant test model. Whereas sensitization after allergen exposure (leading eventually to allergic contact dermatitis (ACD)) has been extensively described in the literature e.g. penetration of chemicals through the stratum corneum, activation of keratinocytes, maturation and migration of LC to the draining lymph nodes and stimulation of T cell responses (Roggen, 2014), extremely little is known about the mechanisms resulting in irritant contact dermatitis (ICD). Clearly, a localized acute inflammatory reaction is involved. Furthermore, it has been shown that the number of CD1a positive cells decreases in both the epidermis and dermis in ICD (Jacobs et al., 2006;Marks et al., 1987). Until now, the fate of these migrated LC was unknown.

[61] Animal Models of Contact Dermatitis

  • Authors: F. Simonetta, C. Bourgeois
  • Year: 2011
  • Venue: Unknown venue
  • URL: https://www.semanticscholar.org/paper/51e0c65da823cb43f6bbb1fd5dab1e08309fcdb8
  • DOI: 10.5772/29462
  • Citations: 5
  • Influential citations: 1
  • Summary: The respective role of innate and adaptive immune cells in contact dermatitis pathogenesis as revealed by murine studies is highlighted and molecular pathways which are promising candidates as targets of future biological therapies are reviewed.
  • Evidence snippets:
  • Snippet 1 (score: 0.402) > Contact dermatitis is an inflammatory disease of the skin resulting from direct contact with foreign substances. Understanding the immunological processes that cause the disease is therefore essential for the development of new therapeutic strategies. Murine models of chemically induced dermatitis have played an essential role in our understanding of the pathophysiology of contact dermatitis, unraveling the role played by inflammatory mediators and identifying potential targets for therapeutic interventions. In the present chapter we review data obtained in animal models of allergic and irritant contact dermatitis and provide basic protocols to reliably induce contact dermatitis. A major intent of this chapter is to highlight the respective role of innate and adaptive immune cells in contact dermatitis pathogenesis as revealed by murine studies. Through genetic ablation of single molecules or depletion of specific cell subsets, murine studies provide novel insight on the role of different components of the immune system in the development of contact dermatitis. We review the experimental evidence revealing the role of different T cell subsets in contact dermatitis development, focusing our attention on mechanisms responsible for maintenance or disruption of immune-tolerance. Our analyses will focus on molecular pathways which are promising candidates as targets of future biological therapies.

[62] Weak Sensitizers May Be Associated with CD80 Polymorphisms: Implications for Systemic Contact Dermatitis

  • Authors: Susan T Nedorost, Ge Zhang, D. Fekedulegn, Kara Fluharty, Wei Wang et al.
  • Year: 2025
  • Venue: JID Innovations
  • URL: https://www.semanticscholar.org/paper/44815e8fb97eb7d3bd2dc6a2fb39054e8bab680b
  • DOI: 10.1016/j.xjidi.2025.100382
  • PMID: 40519868
  • PMCID: 12167014
  • Citations: 2
  • Summary: It was found that positive patch tests to weak allergens were common with 3 polymorphisms of CD80, and ILC2 presentation may bypass education in the local lymph node, explaining the association of antigens classified as non-sensitizers in LLN assay with CD80, and the absence of symptoms of immediate type hypersensitivity in many of these patients.
  • Evidence snippets:
  • Snippet 1 (score: 0.402) > DE is also associated with IgG administration (Voland et al, 2023). > We explored genetic variants important in cutaneous immunology in adult patients with clinically relevant positive patch tests at 2 tertiary, referral contact dermatitis clinics. We stratified patients with a history of early childhood flexural dermatitis as a marker for genetic barrier defects predisposing to chronic irritant dermatitis and patients with a history of DE. > Because innate signals from irritant dermatitis instruct the adaptive response, we also compared our genetic variant associations in this group of patients with ACD with a previously reported cohort of healthcare workers with and without chronic irritant hand dermatitis, analyzed using the same methods (Yucesoy et al, 2016). This allowed us to differentiate genetic variants important in the prerequisite irritant contact dermatitis from those facilitating sensitization to various groups of contact allergens. > Our a priori groupings for allergens on the standard screening series were intended to explore multiple hypotheses at once, including different antigen presentation for metal allergens, immunological differences in antigens metabolized in the skin, differences in polysensitized patients (sensitized to 3 or more chemically unrelated allergens), and differences in patients sensitized to weak antigens. In this study, we explored only the weak allergens (propylene glycol, vanillin, eugenol, and paraben mix); there are many other weak allergens in foods and food additives, but these were chosen because they were included on the standard screening series at both study sites. > We show all the 1450 genetic markers that we explored in the complete dataset (Nedorost et al, 2025). Because of the large number of markers studied, none of the individual analyses survived Bonferroni correction for tests of multiple associations, including the strongest association noted, which was between IL-4R and AD. The latter is well-accepted, and we looked for other associations with similar P-values (P < .005) and ORs (!1.8 or 0.5).

[63] Machine-learning–driven biomarker discovery for the discrimination between allergic and irritant contact dermatitis

  • Authors: V. Fortino, L. Wisgrill, P. Werner, S. Suomela, Nina Linder et al.
  • Year: 2020
  • Venue: Proceedings of the National Academy of Sciences of the United States of America
  • URL: https://www.semanticscholar.org/paper/8cd6f0fb1b6d9cb9edb2e144d4436f98efeb1c9f
  • DOI: 10.1073/pnas.2009192117
  • PMID: 33318199
  • PMCID: 7776829
  • Citations: 64
  • Influential citations: 3
  • Summary: This study identifies and validates biomarkers to distinguish allergic and irritant contact dermatitis in human skin, to be used for the development of novel diagnostic methods and to guide clinical diagnosis of contact allergies.
  • Evidence snippets:
  • Snippet 1 (score: 0.398) > Significance Contact dermatitis is an inflammatory skin disorder that arises from direct skin contact with irritants or allergens. Representing over 90% of occupational skin disorders, it has a considerable socioeconomic impact, and patients suffering from contact dermatitis can develop a notable physical handicap. Current diagnostic regimes rely on allergy testing, exposure specification, and follow-up visits. However, distinguishing the clinical phenotype of irritant and allergic contact dermatitis, which is important for appropriate therapeutic strategies, remains challenging. This study identifies and validates biomarkers to distinguish allergic and irritant contact dermatitis in human skin, to be used for the development of novel diagnostic methods and to guide clinical diagnosis. Contact dermatitis tremendously impacts the quality of life of suffering patients. Currently, diagnostic regimes rely on allergy testing, exposure specification, and follow-up visits; however, distinguishing the clinical phenotype of irritant and allergic contact dermatitis remains challenging. Employing integrative transcriptomic analysis and machine-learning approaches, we aimed to decipher disease-related signature genes to find suitable sets of biomarkers. A total of 89 positive patch-test reaction biopsies against four contact allergens and two irritants were analyzed via microarray. Coexpression network analysis and Random Forest classification were used to discover potential biomarkers and selected biomarker models were validated in an independent patient group. Differential gene-expression analysis identified major gene-expression changes depending on the stimulus. Random Forest classification identified CD47, BATF, FASLG, RGS16, SYNPO, SELE, PTPN7, WARS, PRC1, EXO1, RRM2, PBK, RAD54L, KIFC1, SPC25, PKMYT, HISTH1A, TPX2, DLGAP5, TPX2, CH25H, and IL37 as potential biomarkers to distinguish allergic and irritant contact dermatitis in human skin. Validation experiments and prediction performances on external testing datasets demonstrated potential applicability of the identified biomarker models in the clinic. Capitalizing on this knowledge, novel diagnostic tools can be developed to guide clinical diagnosis of contact allergies.

[64] Immunopathology of allergic contact dermatitis.

[65] Transcriptomic Analysis of Allergic Patch Test Reactions in Non‐Atopic Patients: A Comparative Study Across Multiple Allergens

  • Authors: D. Pesqué, Evelyn Andrades, Pau Berenguer-Molins, J. Perera-Bel, Miquel Clarós et al.
  • Year: 2025
  • Venue: Allergy
  • URL: https://www.semanticscholar.org/paper/3b31c17b9eadd782b5ada96175be429b063769a4
  • DOI: 10.1111/all.16642
  • PMID: 40632077
  • PMCID: 12590323
  • Citations: 3
  • Summary: Molecular signatures and their immune mechanisms of different relevant allergens are characterized and their immune mechanisms of different relevant allergens are characterized in strong and extreme positive patch test reactions of patients without atopic dermatitis.
  • Evidence snippets:
  • Snippet 1 (score: 0.388) > Allergic contact dermatitis (ACD) is a common inflammatory condition due to a type IV delayed hypersensitivity response [1]. ACD diagnosis requires performing patch testing, which induces a reaction to the culprit sensitizer [2]. Different animal and human studies have investigated the various mechanisms involved in different phases of ACD. Mechanisms in the sensitization phase have been extensively characterized, whereas immune mechanisms underlying elicitation have yet to be completely elucidated [3]. With respect to elicitation, molecular studies have revealed a double-faceted nature of this condition [4][5][6][7][8]. The presence of common biomarkers and pathways among different allergens in both patch-induced ACD and clinical ACD lesions has been described, with potential application to distinguish ACD from other conditions, including irritant contact dermatitis [4,6]. However, molecular profiling has also shown allergen-dependent immune responses that could contribute to a specific polarization induced by allergen [5]. The number of allergen-specific differentially expressed genes (DEG) may even exceed the number of shared ACD biomarkers [4,5]. > To date, there has been discordance in the immune transcriptomic pathways involved in ACD lesions, particularly in relation to adaptive immune responses [4,5,8]. Several factors, including comorbid skin conditions and reaction severity, may influence the immunological mechanisms in transcriptomic skin studies for ACD. In this regard, atopic dermatitis has been shown to attenuate ACD immune reactions with subsequently altered polarization in patch test studies [9]. Previous studies have demonstrated that more severe patch test reactions may be associated with specific pathologic characteristics [10,11], changes in the phenotype of peripheral blood T cells [12], and detected more dysregulated genes [4].

Notes

  • This provider combines search_papers_by_relevance with snippet_search.
  • No synthesis or second-stage model call is performed.