Atopic Dermatitis Management: from Conventional Therapies to Biomarker-Driven Treatment Approaches

Abstract

Atopic dermatitis (AD) is a chronic relapsing inflammatory skin disorder characterized by pruritus, skin barrier dysfunction, and immune dysregulation. It significantly impacts the quality of life and increases the risk of infections, sleep disturbances, and psychological distress. AD pathogenesis involves genetic predisposition, environmental triggers, microbiome alterations, and immune dysfunction. Traditional treatments such as topical corticosteroids, calcineurin inhibitors, and systemic immunosuppressants provide symptomatic relief but often fail to provide long-term disease control. The emergence of targeted biologics and Janus kinase inhibitors has transformed AD management by offering more precise and effective therapeutic options. However, treatment responses vary, highlighting the need for biomarker-driven personalized therapies. In this review, we explore the evolving therapeutic landscape of AD, emphasizing the emerging role of biomarker-guided treatment strategies. We highlight recent discoveries of therapeutic (OX40, IgE, IL-5, IL-31, IL-22, thymic stromal lymphopoietin) and diagnostic (TARC/CCL17, MDC/CCL2, filaggrin, sphingosine-1-phosphate, CXCL2) biomarkers that offer promising avenues for patient stratification and treatment monitoring. This review offers novel insight into how the convergence of biomarker research and therapeutic innovation can address current gaps in AD care. Future research should focus on refining biomarker-guided treatment strategies, optimizing therapeutic combinations, and addressing unmet patient needs. The integration of biomarker-guided strategies into routine clinical practice represents a critical step toward long-term disease control and improved quality of life for AD patients.

Keywords: Atopic dermatitis; Biomarkers; Conventional treatment; Precision medicine; Targeted therapies.

Fig. 1

A comprehensive overview of atopic dermatitis (AD) management, illustrating conventional therapies and biomarker-driven treatments. Conventional therapies include topical agents, systemic corticosteroids, and systemic treatments such as monoclonal antibodies, Janus kinase (JAK) inhibitors, and antimetabolites. Biomarker-driven treatments focus on therapeutic and diagnostic biomarkers, which play a crucial role in targeted therapy and personalized treatment approaches for AD.

Fig. 2

Schematic representation of the pathophysiology of atopic dermatitis and the mechanisms of action of key conventional and biomarker-driven therapies. The disease is characterized by skin barrier disruption, allergen penetration, and microbial colonization, leading to Th2-dominant immune activation and cytokine overproduction. The left panel highlights targeted therapies which include monoclonal antibodies and biologics (e.g., dupilumab, tralokinumab, lebrikizumab, fezakinumab, omalizumab, ligelizumab, tezepelumab, amlitelimab, telazorlimab, rocatinlimab, nemolizumab, mepolizumab, benralizumab), small molecule inhibitors (e.g., JAK inhibitors, PDE4 inhibitors), and conventional treatments, such as topical corticosteroids and calcineurin inhibitors. The right panel depicts antimetabolites used in conventional systemic therapy, such as cyclosporine, methotrexate, azathioprine, and mycophenolate mofetil, which broadly suppress T-cell activation and proliferation. Together, these therapies target distinct immune pathways, ranging from broad immunosuppression to biomarker-driven precision medicine in atopic dermatitis management. S. aureus, Staphylococcus aureus; Th, T helper cell; IL, interleukin; TSLP, thymic stromal lymphopoietin; PDE4, phosphodiesterase-4; IgE, immunoglobulin E; IMPDH, inosine monophosphate dehydrogenase; NFAT, nuclear factor of activated T-cells; AICAR IMP, 5-aminoimidazole-4-carboxamide ribonucleotide transformylase/inosine monophosphate; DHFR, dihydrofolate reductase.