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Review
. 2025 Mar 13:6:1564528.
doi: 10.3389/falgy.2025.1564528. eCollection 2025.

Scratching the surface: biomarkers and neurobiomarkers for improved allergic contact dermatitis management

Akimi Sasaki #  1 , Manuel Sargen #  1 , Anish R Maskey #  1 , Xiu-Min Li  1   2   3
Affiliations
Review

Scratching the surface: biomarkers and neurobiomarkers for improved allergic contact dermatitis management

Akimi Sasaki et al. Front Allergy. .

Abstract

Allergic contact dermatitis (ACD), also known as allergic eczema, is a common inflammatory skin disorder that affects millions of Americans and imposes significant physical, psychological, and economic burdens. Differentiating ACD from other forms of dermatitis remains a challenge, with patch testing as the gold standard. Despite its utility, patch testing can lack diagnostic accuracy, highlighting the importance of molecular biomarkers to refine diagnosis and treatment. Advances in transcriptomics and machine-learning have enabled the identification of biomarkers involved in ACD, such as loricrin (LOR), ADAM8, CD47, BATF, SELE, and IL-37. Moreover, biomarkers such as LOR, NMF, and TEWL, may have prognostic value in evaluating therapeutic response. Emerging neurological biomarkers (neurobiomarkers), including IL-31 and TRPV1, target pathways involved in the pruritic and inflammatory responses, offering novel therapeutic targets as well. This mini review summarizes current ACD treatments, biomarkers for targeted therapies, and emphasizes the role of neurobiomarkers in ACD treatment. Additional research on the validity of the therapeutic potential of these biomarkers is necessary to improve ACD treatment and outcomes.

Keywords: IL-31; allergic contact dermatitis; inflammation; neurobiomarkers; pruritus.

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Conflict of interest statement

XL received grants to her institution from the National Institutes of Health, Food Allergy Research and Education (FARE), Winston Wolkoff Integrative Medicine Fund for Allergies and Wellness, the Parker Foundation, New York State Department of Health, the Lie-Artati Family Fund and Fidelity Charitable DAS Fund; received consultancy fees from FARE, Johnson & Johnson Pharmaceutical Research & Development, L.L.C, Bayer Global Health LLC; received royalties from UpToDate; shares US patent US7820175B2, US10500169B2, US10406191B2, US10028985B2, US11351157B2; takes compensation from her practice at the Center for Integrative Health and Acupuncture PC; Her related party manages US Times Technology Inc; is a cofounder of General Nutraceutical Technology LLC. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Pathophysiology of ACD and associated neuro biomarkers. The pathophysiology of ACD involves a two-phase immune response. (A) In the sensitization phase, allergens/haptens penetrate the skin, form hapten-self-protein complexes, and are processed by dendritic cells (DCs), promoting T-cell priming in lymphoid tissue. (B,C) The elicitation phase occurs upon re-exposure to the allergen, activating effector and memory T-cells that migrate to the skin, causing inflammation, erythema, or spongiosis. (D) Peptidergic neurons sustain inflammation by releasing neuropeptides that activate mast cells, promote DC migration, and enhance T-cell priming. TRPV1, an ion channel expressed on peptidergic neurons, contributes to inflammatory signaling. (E) Nonpeptidergic neurons, especially the NP3 subset, express the IL-31 receptor (IL-31R) complex, and are activated during allergen re-exposure to maintain itch perception. (F) IL-31, a pruritogenic cytokine, is secreted by activated T-cells and mast cells, amplifying itch and inflammation. (G) The combined immune and neural pathways drive the clinical features of ACD, namely chronic itch. (Created with BioRender).
See this image and copyright information in PMC

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