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

Autor:in

Cabezas-Cruz, Alejandro; Hodzic, Adnan; Hernández, Lourdes; Contreras Rojo, Marinela; de la Fuente, José

Abstrakt

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 alpha Gal syndrome (AGS) a type of allergy characterized by an IgE response against the carbohydrate Gal alpha 1-3Gal (alpha-Gal). This glycan is present in tick salivary proteins and on the surface of tick-borne pathogens such as Bo,,elia bu,gdo,fe,i and Anaplasma phagocytophilum the causative agents of Lyme disease and granulocytic anaplasmosis. Most alpha-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 alpha-Gal sensitization allergy and the AGS. We propose that the alpha-Gal-specific IgE response in humans is an evolutionary adaptation associated with ATR and allergic klendusity with the trade-off of developing AGS.

Dokumententyp

Übersichtsarbeit

DOI

10.1042/BCJ20200915

PubMed ID

MEDLINE:33988703