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IgE in horses: occurrence in health and disease.
Vet Immunol Immunopathol. 2009 Nov 15; 132(1):21-30.VI

Abstract

Since the initial characterization of IgE by Ishizaka et al. (1966), IgE was described in several mammalian species. In horses, a single gene encoding the IgE heavy chain constant region (IGHE gene) exists per haploid genome and several allelic variants of the equine IGHE gene were found. IgE occurs in its soluble form in equine serum and physiological concentrations of total IgE are around 1000-fold higher in normal horse than in normal human serum. Maternal IgE is enriched in the colostrum and transferred to the neonatal foal after birth. Foals do not produce detectable concentrations of endogenous IgE for several months after birth. IgE is also found on the surface of a small percentage of equine peripheral blood cells including basophils, and subpopulations of B-cells and monocytes, and on mast cells in various tissues such as the skin, and the submucosa of the airways and intestine. Both, the high- and low-affinity IgE receptor genes are identified in the horse suggesting binding of soluble IgE from the circulation to these receptors. Horses naturally develop type I hypersensitivities. IgE-mediated mechanisms were implicated in the pathogenesis of several allergic diseases in horses since almost 30 years. The findings were mainly based on the induction of immediate skin reactions after intradermal testing with allergen extracts. With the development of the first monoclonal antibodies to equine IgE within the past years, more insights into the pathogenesis of allergic diseases could be obtained. Today, various techniques are available to detect soluble IgE and the sensitization of mast cell or basophils with IgE in horses. An IgE-mediated allergic etiology is confirmed for skin hypersensitivity. The causing role of IgE in other diseases such as recurrent airway obstruction (RAO) still remains controversial. More recent studies did not confirm an IgE-mediated pathogenesis of RAO. This suggested that the disease is a chronic inflammatory condition with some indication for an involvement of delayed-type hypersensitivity mechanisms. In summary, our knowledge about the role of IgE during the immune response of the horse improved tremendously during the past decade. New IgE-specific tools and technologies are likely to uncover additional aspects of IgE-mediated mechanisms in equine health and disease.

Authors+Show Affiliations

Department of Population Medicine and Diagnostic Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA. bw73@cornell.edu

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

19819562

Citation

Wagner, Bettina. "IgE in Horses: Occurrence in Health and Disease." Veterinary Immunology and Immunopathology, vol. 132, no. 1, 2009, pp. 21-30.
Wagner B. IgE in horses: occurrence in health and disease. Vet Immunol Immunopathol. 2009;132(1):21-30.
Wagner, B. (2009). IgE in horses: occurrence in health and disease. Veterinary Immunology and Immunopathology, 132(1), 21-30. https://doi.org/10.1016/j.vetimm.2009.09.011
Wagner B. IgE in Horses: Occurrence in Health and Disease. Vet Immunol Immunopathol. 2009 Nov 15;132(1):21-30. PubMed PMID: 19819562.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - IgE in horses: occurrence in health and disease. A1 - Wagner,Bettina, Y1 - 2009/09/23/ PY - 2009/10/13/entrez PY - 2009/10/13/pubmed PY - 2010/1/12/medline SP - 21 EP - 30 JF - Veterinary immunology and immunopathology JO - Vet Immunol Immunopathol VL - 132 IS - 1 N2 - Since the initial characterization of IgE by Ishizaka et al. (1966), IgE was described in several mammalian species. In horses, a single gene encoding the IgE heavy chain constant region (IGHE gene) exists per haploid genome and several allelic variants of the equine IGHE gene were found. IgE occurs in its soluble form in equine serum and physiological concentrations of total IgE are around 1000-fold higher in normal horse than in normal human serum. Maternal IgE is enriched in the colostrum and transferred to the neonatal foal after birth. Foals do not produce detectable concentrations of endogenous IgE for several months after birth. IgE is also found on the surface of a small percentage of equine peripheral blood cells including basophils, and subpopulations of B-cells and monocytes, and on mast cells in various tissues such as the skin, and the submucosa of the airways and intestine. Both, the high- and low-affinity IgE receptor genes are identified in the horse suggesting binding of soluble IgE from the circulation to these receptors. Horses naturally develop type I hypersensitivities. IgE-mediated mechanisms were implicated in the pathogenesis of several allergic diseases in horses since almost 30 years. The findings were mainly based on the induction of immediate skin reactions after intradermal testing with allergen extracts. With the development of the first monoclonal antibodies to equine IgE within the past years, more insights into the pathogenesis of allergic diseases could be obtained. Today, various techniques are available to detect soluble IgE and the sensitization of mast cell or basophils with IgE in horses. An IgE-mediated allergic etiology is confirmed for skin hypersensitivity. The causing role of IgE in other diseases such as recurrent airway obstruction (RAO) still remains controversial. More recent studies did not confirm an IgE-mediated pathogenesis of RAO. This suggested that the disease is a chronic inflammatory condition with some indication for an involvement of delayed-type hypersensitivity mechanisms. In summary, our knowledge about the role of IgE during the immune response of the horse improved tremendously during the past decade. New IgE-specific tools and technologies are likely to uncover additional aspects of IgE-mediated mechanisms in equine health and disease. SN - 1873-2534 UR - https://www.unboundmedicine.com/medline/citation/19819562/IgE_in_horses:_occurrence_in_health_and_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0165-2427(09)00314-6 DB - PRIME DP - Unbound Medicine ER -
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