Immunoglobulin‐E‐bearing cells in skin biopsies of horses with insect bite hypersensitivity

Abstract

Summary The aim of the present study was to investigate, with immunohistochemistry and in situ hybridisation, if immunoglobulin‐E (IgE) and mast cells are involved in the pathogenesis of insect bite hypersensitivity (IBH), an allergic dermatitis of horses. In tissue sections fixed in paraformaldehyde (PFA) for <24 h, significantly more IgE protein‐bearing cells were found in the dermis and epidermis of acute and chronic IBH lesions than in skin biopsies from healthy horses (medians = 466, 236 and 110 cells/mm2, respectively; P ≤ 0.01). More IgE‐mRNA positive (+) cells were observed in the dermis of acute IBH lesions than in the dermis of healthy skin (median = 2.8 vs. 0.0 cells/mm2; P ≤ 0.01). Significantly, more mast cells were detected with metachromatic (median = 160 vs. 62 cells/mm2; P ≤ 0.001) and tryptase‐specific stainings (median = 120 vs. 69 cells/mm2; P ≤ 0.001) in the dermis of acute IBH biopsies compared to healthy skin. No chymase+ mast cells were found in any skin biopsy. IBH lesions fixed in PFA for >24 h were compared to dermatomycosis (DM) lesions; IBH biopsies contained a similar number of IgE‐protein+ cells to DM biopsies (median = 249 vs. 192 cells/mm2; P = 0.08) but had significantly more IgE‐mRNA+, metachromatic and tryptase+ mast cells than DM biopsies. This study suggests an involvement of IgE‐mediated immune reactions in the pathogenesis of IBH as well as, sometimes, in dermatomycosis. Using double labelling, cells which expressed IgE protein and contained mast cell enzymes were detected.

Phenotype and function of IgE-binding monocytes in equine Culicoides hypersensitivity

“…One possible explanation for the differences between prior human studies and our horse study could be due to uncontrolled variables inherent to human cohorts. Similar uncontrolled variables, differences in housing environments, and seasonal variation between sample collection timepoints also applied to previous horse studies on Cul hypersensitivity [2,10,12,[16][17][18]. In our study, the use of the equine model allowed the study of a naturally occurring allergic response in a controlled environment (same geographic location, housing conditions, diet, vaccination and deworming schedules) with comparable Cul exposure between all horses.…”

“…Reactions range in severity and can be debilitating for the horse. This hypersensitivity reaction is mediated by the production of IgE and subsequent sensitization of mast cells and basophils by binding of IgE to the high-affinity IgE receptor (FcεRI) on the surface of these cells [10][11][12][13][14][15][16]. Exposure to allergen induces crosslinking of allergen-specific IgE/FcεRI complexes on mast cells, resulting in rapid degranulation and an immediate inflammatory response [17,18].…”

The same ELA class II risk factors confer equine insect bite hypersensitivity in two distinct populations

“…However, other immunological reactions, such as delayed type IV hypersensitivity, cannot be excluded during the chronic stages of the disease (Fadok and Greiner 1990). Skin sections reveal infiltration of eosinophils and mast cells as well as increased numbers of IgE-bearing cells, an increased total number of T cells and expression of T helper cells (Th2) (Van der Haegen et al 2001; Heimann et al 2011). Clinical signs include intensely pruritic lesions, urticaria, oedema and papules (Baker and Quinn 1978; Halldordsottir and Larsen 1991).…”

Recombinant Culicoides obsoletus complex allergens stimulate antigen‐specific T cells of insect bite hypersensitive Shetland ponies in vitro

“…Various studies have shown that IBH is an IgE‐mediated allergy that resembles type I allergies in humans . In addition, there is evidence for the involvement of Th1‐, Th2‐ and regulatory T (Treg)‐type cytokines in IBH in Icelandic horses .…”