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Eosinophils are multifunctional granulocytes central to type 2 inflammation, allergy and host defence. In dermatology, their presence is frequent, either as a secondary finding in well-defined inflammatory disorders or, more rarely, as the defining feature of primary eosinophilic dermatoses. The pathogenic role of eosinophils is linked to their ability to release toxic granule proteins, lipid mediators, cytokines and extracellular traps, which contribute to both host protection and tissue damage. Their activation is orchestrated by cytokines such as interleukin (IL)-3, IL-5 and granulocyte–macrophage colony-stimulating factor, and by chemokines including eotaxins, which ensure selective recruitment to inflamed tissues such as the skin. This review provides an updated overview of eosinophils in cutaneous disease. It delineates the spectrum of eosinophil-associated dermatoses, ranging from common disorders such as atopic dermatitis, chronic urticaria, bullous pemphigoid and drug hypersensitivity syndromes, to rare primary eosinophilic dermatoses including Wells syndrome, eosinophilic pustular folliculitis, and recurrent cutaneous eosinophilic vasculitis. These entities are clinically and histologically heterogeneous, may overlap with systemic hypereosinophilic syndromes, and often present diagnostic and therapeutic challenges. Beyond their direct cytotoxicity, eosinophils also contribute to fibrosis, immune regulation and potentially tumour surveillance. Recognizing their central role provides new perspectives for classification and management. Therapeutic strategies range from conventional corticosteroids to emerging targeted therapies, including monoclonal antibodies against IL-5 and IL-5R, and dupilumab targeting the type 2 pathway. By framing eosinophilic skin conditions within the broader concept of eosinophilic disorders, this review emphasizes the importance of early recognition, multidisciplinary evaluation and personalized therapeutic approaches to improve patient outcomes.
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Dezoteux et al. (2026) studied this question.
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