Project

Immunotherapies for insect bite hypersensitivity (IBH) in horses

Insect bite hypersensitivity (IBH), also known as summer eczema, is the most common skin allergy affecting horses worldwide. IBH is caused by the bites of (mainly) Culicoides obsoletus midges. In horses that develop IBH, the bites induce an allergic reaction with intense itch, swelling, hair loss and skin thickening. Self-inflicted wounds occur when horses scratch harshly.

Within our project we work on developing immunotherapies aiming to cure IBH, based on the understanding of the immune mechanisms behind this allergy.

Background

Insect bite hypersensitivity (summer eczema, sweet itch) is the most common allergic dermatitis compromising health and welfare of horses worldwide. IBH is caused by the bites of midges, mainly from the complex. In allergic horses, the bites of these midges induce an allergic reaction that results in intense itch, oedema, alopecia (hair loss) and lichenification (thickening) of the skin. Secondary wounds and even self-mutilation occurs when horses scratch to relieve their itch. Unfortunately there is no curative treatment for IBH.

IBH is a skin allergy that involves an IgE mediated type I hypersensitive reaction (Figure 1). In horses that develop IBH, the first exposure to midge allergens triggers a T helper-2 (Th2) type response that promotes the production of allergen-specific antibodies of the IgE isotype. These IgE antibodies bind with their constant part to high-affinity IgE receptors (FcεR I) on mast cells and basophils (sensitization). Upon re exposure to the allergen, the contact of this allergen with the allergen-specific IgE antibodies on mast cells and basophils provokes the release of large amounts of allergy mediators (e.g. histamine) that induce a local allergic reaction in the skin.

Figure 1. Immune mechanism of Insect bite hypersensitivity. IBH involves an IgE mediated type 1 hypersensitive reaction. In horses that develope IBH, the first exposure to midge allergens triggers a T helper type 2 (Th2) response that promotes the production of allergen-specific antibodies of the IgE isotype. These IgE antibodies bind with their constant part to high-affinity IgE receptors (FceR 1) on mast cells and basophils (sensitisation). Upon re-exposure, allergens bind to two specific IgE antibodies on mast cells and basophils (cross-linking) and provoke the release of large amounts of allergy mediators (e.g. histamine). These mediators induce the local allergic reaction in the skin.

The project

Based on the immune mechanism behind this skin allergy, we design and test allergen specific immunotherapy strategies to modify the allergic response towards Culicoides obsoletusallergens into a non-allergic one, with the aim of curing horses allergic to these midges.

Publications