Abstract

BackgroundEpicutaneous sensitization with protein allergen that induces predominant Th2 responses is an important sensitization route in atopic dermatitis. Fungal components have been shown to modulate Th cell differentiation. However, the effects of fungal components on epicutaneous sensitization are unclear.ResultsIn this study, we showed that co-administration of curdlan, a dectin-1 agonist, during epicutaneous ovalbumin sensitization of BALB/c mice decreased the IL-5 and IL-13 levels in supernatants of lymph node cell ovalbumin reactivation cultures. Mechanistically, curdlan co-administration decreased IL-4 and IL-1β expressions in draining lymph nodes. Curdlan co-administration also lower the migration of langerin+ CD103- epidermal Langerhans cells into draining lymph nodes at 96 hours post-sensitization which might be attributed to decreased expressions of IL-18 and IL-1β in patched skin. Moreover, adoptive transfer of CFSE-labeled transgenic CD4 T cells confirmed that curdlan co-administration decreased the proliferation and IL-4-production of ovalbumin -specific T cells primed by epidermal Langerhans cells.ConclusionsThese results indicated that concurrent exposure to a dectin-1 agonist suppresses the epicutaneously induced Th2 response by modulating the cytokine expression profiles in draining LNs and the migration of epidermal Langerhans cells. These results highlight the effects of fungal components on epicutaneous allergen sensitization in atopic diseases.

Highlights

  • Epicutaneous sensitization with protein allergen that induces predominant Th2 responses is an important sensitization route in atopic dermatitis

  • Co-administration of a dectin-1 agonist suppresses the predominant Th2 response induced by epicutaneous sensitization with protein antigen Curdlan is a (1–3) β-glucan that activates dectin-1 signaling

  • The levels of IFN-γ and IL-17 in the supernatants for these groups of mice were again variable compared to mice that received OVA alone. These results indicate that co-administration of a dectin-1 agonist, including curdlan and zymosan, suppresses the predominant Th2 response induced by epicutaneous sensitization with protein antigen

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Summary

Introduction

Epicutaneous sensitization with protein allergen that induces predominant Th2 responses is an important sensitization route in atopic dermatitis. Fungal components have been shown to modulate Th cell differentiation. The effects of fungal components on epicutaneous sensitization are unclear. The prevalence of atopic diseases has progressively increased in recent decades. The interaction between genetic susceptibility for atopy with varying environmental allergen exposures plays a central role in the pathogenesis of atopic diseases [1]. Allergens that provoke atopic diseases are ubiquitously distributed environmental protein antigens. The route of protein allergen sensitization in AD remains unclear. Compelling clinical evidence suggests that epicutaneous exposure to protein antigen expected to be a useful strategy to modulate the natural course of atopic diseases [12]

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