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Tick–human interactions: from allergic klendusity to the α-Gal syndrome

Abstract : Ticks and the pathogens they transmit, including bacteria, viruses, protozoa, and helminths, constitute a growing burden for human and animal health worldwide. The ability of some animal species to acquire resistance to blood-feeding by ticks after a single or repeated infestation is known as acquired tick resistance (ATR). This resistance has been associated to tick-specific IgE response, the generation of skin-resident memory CD4+ T cells, basophil recruitment, histamine release, and epidermal hyperplasia. ATR has also been associated with protection to tick-borne tularemia through allergic klendusity, a disease-escaping ability produced by the development of hypersensitivity to an allergen. In addition to pathogen transmission, tick infestation in humans is associated with the α-Gal syndrome (AGS), a type of allergy characterized by an IgE response against the carbohydrate Galα1-3Gal (α-Gal). This glycan is present in tick salivary proteins and on the surface of tick-borne pathogens such as Borrelia burgdorferi and Anaplasma phagocytophilum, the causative agents of Lyme disease and granulocytic anaplasmosis. Most α-Gal-sensitized individuals develop IgE specific against this glycan, but only a small fraction develop the AGS. This review summarizes our current understanding of ATR and its impact on the continuum α-Gal sensitization, allergy, and the AGS. We propose that the α-Gal-specific IgE response in humans is an evolutionary adaptation associated with ATR and allergic klendusity with the trade-off of developing AGS.
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https://hal.inrae.fr/hal-03314572
Contributor : Camille Serva <>
Submitted on : Thursday, August 5, 2021 - 10:16:54 AM
Last modification on : Friday, August 6, 2021 - 3:35:15 AM

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Alejandro Cabezas Cruz, Adnan Hodžić, Lourdes Mateos-Hernández, Marinela Contreras, José de la Fuente. Tick–human interactions: from allergic klendusity to the α-Gal syndrome. Biochemical Journal, Portland Press, 2021, 478 (9), pp.1783-1794. ⟨10.1042/BCJ20200915⟩. ⟨hal-03314572⟩

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