Valgerður Andrésdóttir, Ólöf Sigurðardóttir and Einar Jörundsson, Institute for Experimental Pathology, University of Iceland, Keldur. Eliane Marti and Eman Hamza, Dept. of Clin. Vet. Med. Vetsuisse Faculty University of Berne Switzerland, Reto Crameri SIAF, Davos, Switzerland, Einar Mäntylä, Jón Már Björnsson and Arna Rúnarsdóttir ORF Genetics, Bettina Wagner, Dept. of Population Medicine and Diagnostic Sciences College of Veterinary Medicine Cornell University, Ithaca, NY USA, Einar Torfason Department of Virology the University Hospital, Sigríður Björnsdóttir, Chief veterinary office, Selfoss, Iceland, Sveinn Steinarsson, the Horse farmers association
Insect bite hypersensitivity
Insect bite hypersensitivity (IBH) or summer eczema (SE) is a dermatitis of horses, caused by IgE mediated hypersensitivity reaction, to Culicoides spp. (biting midges) not indigenous to Iceland (Schaffartzik et al., 2012). All breeds of horses can be affected, but Icelandic horses born in Iceland and exported to the continent are more strongly affected than most other breeds (Bjornsdottir et al., 2006). Since the year 2000 there has been an ongoing collaborative project between Keldur and the University of Berne, Switzerland. The aim of the project is to find and characterize the allergens causing IBH and analyse the immune response that leads to the disease and the final aim is development of immunotherapy against insect bite hypersensitivity.
Numerous allergen genes, originated in the salivary glands of three Culicoides species have been isolated and the proteins expressed in E. coli (Langer et al., 2009, Schaffartzik et al., 2010 and 2011; van der Meide et al., 2013, Peeters et al., 2013) Several of the allergens have also been expressed in insect cells (Stefánsdóttir 2015) and three in barley.
Th2 type, IgE mediated reactions are involved to a much stronger extent in Icelandic horses than in some other breeds and after export there is an imbalance between Th1, Th2 and T regulatory cells (Treg) (Hamza et al., 2010; Hamza et al., 2008; Heimann et al., 2011). It should therefore be possible to rebalance the Th1:Th2:Treg responses and restraint the inflammatory mechanisms by strengthening the Treg response against the allergens using allergen specific immunotherapy.