Interleukin‐33 modulates the expression of human β‐defensin 2 in human primary keratinocytes and may influence the susceptibility to bacterial superinfection in acute atopic dermatitis

Abstract

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Skin Barrier Dysfunction and Low Antimicrobial Peptide Expression in Cutaneous T-cell Lymphoma

“…Table 1. Filaggrin, loricrin, S100A7, and S100A8 expression in lesional skin of patch, plaque, tumor, erythroderma of CTCL, atopic dermatitis, psoriasis and in normal skin filaggrin loricrin S100A7 S100A8 Normal 5 0% 40% 60% 0% 40% 60% 80% 20% 0% 80% 20% 0% CTCL (patch) 5 20% 60% 20% 40% 60% 0% 60% 40% 0% 40% 60% 0% CTCL (plaque) 5 60% 40% 0% 60% 40% 0% 60% 40% 0% 60% 20% 20% CTCL (tumor) 5 80% 20% 0% 80% 20% 0% 60% 40% 0% 40% 60% 0% CTCL (erythroderma) 5 80% 20% 0% 60% 40% 0% 80% 20% 0% 60% 40% 0% Atopic dermatitis 5 80% 20% 0% 80% 20% 0% 40% 60% 0% 60% 40% 0% Psoriasis 5 80% 20% 0% 80% 20% 0% 0% 40% 60% 0% 40% (44)(45)(46). Consistently, in CTCL lesional skin, we detected significant negative correlations between expression levels of S100A7 and those of CCL26 or CCR3, a representative T H 2 chemokine/chemokine receptor pair (Fig.…”

Wounds that heal and wounds that don’t − The role of the IL-33/ST2 pathway in tissue repair and tumorigenesis

“…In recent years, IL-33 has emerged as a key player in several dermatological diseases including psoriasis, atopic dermatitis and contact allergy [52,53]. Recent attention has focussed on exploring the role of both IL-33 and ST2 in cutaneous wound healing.…”

Targeting IL-33 in Autoimmunity and Inflammation

“…IL-33 induces lymphoid cell-mediated airway inflammation by also activating the mammalian target of rapamycin (Salmond et al, 2012). Despite IL-33 sharing the IL-1 receptor accessory protein with other members of the IL-1 family that are known to upregulate an inducible antimicrobial peptide human b-defensin 2 (hBD2), IL-33 downregulates serum-induced hBD2 in human primary keratinocytes; this finding may explain the increased colonization rate of Staphylococcus aureus seen in atopic dermatitis (AD) patients (Alase et al, 2012). Interestingly, hBD2 has been reported to activate human MCs (Subramanian et al, 2013).…”