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.

Keywords: Eosinophil; Granule proteins; Host defense; Immunoregulation; Tissue damage.

Fig. 1

Eosinophil infiltration in the skin. The image shows round shaped eosinophils with their typical bi-lobed nuclei (arrow), cell-free granules indicating degranulation (*), cytolytic eosinophils (arrowhead), and flame figures presenting necrobiotic collagen fibres covered by eosinophil granule proteins (open arrow). Magnification ×400

Fig. 2

Clinical patterns of skin diseases with eosinophilia and examples

Fig. 3

Clinical and histological presentations of dermatoses associated with eosinophilia. Images demonstrate typical skin lesions and pathological findings in H&E stained skin specimens of selected dermatoses with eczematous pattern (A), macular and papular rashes (B), urticarial pattern (C), blister and pustules (D), nodular lesions (E), vasculitis (F), and fibrosis (G). The key clinical and histopathological cutaneous features are the following: (A) Atopic dermatitis: eczema in flexural folds, spongiosis, acanthosis, superficial perivascular lymphohistiocytic infiltrate with eosinophils; scabies: linear burrows, eosinophils are main infiltrating cells; cutaneous T cell lymphoma: eczematous lesions, lymphocytic infiltrate with epidermotropism, occasional eosinophils in dermis; (B) DRESS: widespread erythematous macules and papules, facial edema, unspecific histology, perivascular lymphohistiocytic infiltrate with eosinophils; (C) urticaria: wheals, dermal edema and discrete mixed infiltrate with few eosinophils; eosinophilic cellulitis/dermatitis: urticarial patches; interstitial eosinophil infiltrate, flame figures; (D) bullous pemphigoid: blisters in urticarial or eczematous lesions, subepidermal blisters, numerous eosinophils in the dermis, lining at the dermal–epidermal junction and in blisters; eosinophilic pustular folliculitis: disseminated sterile pustules, intra- and perifollicular eosinophil-rich infiltrate; (E) granuloma faciale: brownish-red nodules and plaques; mixed, eosinophil-rich infiltrates with a grenz zone; angiolymphoid hyperplasia with eosinophilia: grouped violaceous to brownish papules and nodules, proliferation of blood vessels with epitheloid endothelial cell proliferation with cytoplasmic vacuoles, diffuse infiltrate of lymphocytes and numerous eosinophils; (F) esinophilic granulomatosis and polyangiitis: purpuric nodules, intra- and perivascular infiltrate of lymphocytes and eosinophils, destruction of vessel wall, fibrinoid deposition; (G) eosinophilic fasciitis: plate-like hardness of distal limbs, groove sign of blood vessels, thickening of fascia, infiltrate of lymphocytes, plasma cells and eosinophils in early stages