Eosinophils in skin diseases

Abstract

Eosinophil infiltration is a common finding in a broad spectrum of skin diseases, despite the fact that the skin is devoid of eosinophils under physiologic conditions. Although cutaneous eosinophilia is reactive, cytokine-mediated in most cases, diseases with an intrinsic mutation-mediated clonal expansion of eosinophils can also manifest on the skin. As eosinophils are involved in host defense, regulate immune responses, generate pruritus, induce remodeling and fibrosis, and can cause tissue damage, they have the capacity to actively contribute to the pathogenesis of diseases. Recent research provided deeper insights in the mechanisms, e.g., bacterial and viral clearance, blister formation, recruitment of cytotoxic T cells, and generation of pruritus, by which eosinophils might come into action. This review aims at providing an overview on the clinical presentations of eosinophil-associated dermatoses and the current understanding of their pathogenic role in these diseases. Further, we discuss the effects of therapies targeting eosinophils.

Mixed T Helper1/T Helper2/T Cytotoxic Profile in Subjects with Chronic Chagas Disease with Hypersensitivity Reactions to Benznidazole

“…Contrasting with the ELISPOT assays conducted in our study, the lymphocyte transformation test is based on a 6-day culture in which drug-specific T cells are expanded: thus, the sensitivity might be improved, although nonspecific activation of T cells can also occur. The mediators found to increase were previously associated with the clinical manifestations of ADRs to other drugs, including maculopapular rash and exanthema with or without eosinophilia ( 12 , 26 – 28 ). A heterogeneous pattern of cytokines involving CD4 + and CD8 + T cells has been described in ADRs with the development of maculopapular exanthema ( 19 , 29 ), and two cases of overlapping clinical manifestations of drug reaction with eosinophilia and systemic symptoms and Stevens-Johnson syndrome/toxic epidermal necrolysis have been reported in subjects infected with T. cruzi treated with benznidazole ( 30 ).…”

Blood-Based Biomarkers for Eosinophilic Esophagitis and Concomitant Atopic Diseases: A Look into the Potential of Extracellular Vesicles

“…Cytokines released by Th2 lymphocytes (IL-4, IL-5, and IL-13) stimulate, among others things, the proliferation of eosinophils that are subsequently recruited to the inflammatory foci from circulation, causing the eosinophilia characteristic of EoE, BA, and AD [ 32 , 33 , 34 , 35 ]. The cytotoxic nature of eosinophil-granule proteins released locally then promotes skin lesions and pruritus in AD [ 36 ]. As a result, remodeling and hyperresponsiveness of the airways in BA [ 37 ], and esophageal dysmotility and fibrosis in EoE occurs [ 38 ].…”

In vitro models for investigating itch

“…Similar to mast cells, basophils ( Hashimoto et al, 2019 ), eosinophils ( Radonjic-Hoesli et al, 2021 ), neutrophils ( Hashimoto et al, 2018 ), dendritic cells and macrophages all share the ability to release pruritogenic substances and likely contribute to itch ( Toyama et al, 2021 ), especially in immune cell-enriched inflamed skin ( Nguyen and Soulika, 2019 ).…”