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Yoshikawa, Soichiro Department of Cellular Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences ORCID Kaken ID researchmap
Miyake, Kensuke Inflammation, Infection and Immunity Laboratory, TMDU Advanced Research Institute, Tokyo Medical and Dental University (TMDU)
Kamiya, Atsunori Department of Cellular Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Karasuyama, Hajime Inflammation, Infection and Immunity Laboratory, TMDU Advanced Research Institute, Tokyo Medical and Dental University (TMDU)
Abstract
Ticks are blood‐feeding ectoparasites that transmit a variety of pathogens to host animals and humans, causing severe infectious diseases such as Lyme disease. In a certain combination of animal and tick species, tick infestation elicits acquired immunity against ticks in the host, which can reduce the ability of ticks to feed on blood and to transmit pathogens in the following tick infestations. Therefore, our understanding of the cellular and molecular mechanisms of acquired tick resistance (ATR) can advance the development of anti‐tick vaccines to prevent tick infestation and tick‐borne diseases. Basophils are a minor population of white blood cells circulating in the bloodstream and are rarely observed in peripheral tissues under steady‐state conditions. Basophils have been reported to accumulate at tick‐feeding sites during re‐infestation in cattle, rabbits, guinea pigs and mice. Selective ablation of basophils resulted in a loss of ATR in guinea pigs and mice, illuminating the essential role of basophils in the manifestation of ATR. In this review, we discuss the recent advance in the elucidation of the cellular and molecular mechanisms underlying basophil recruitment to the tick‐feeding site and basophil‐mediated ATR.
Keywords
acquired immunity
basophil
histamine
IgE
IL‐3
mast cell
Tick
Published Date
2020-10-30
Publication Title
Parasite Immunology
Volume
volume2021
Issue
issue43
Publisher
Wiley
Start Page
e12804
ISSN
0141-9838
NCID
AA00361321
Content Type
Journal Article
language
English
OAI-PMH Set
岡山大学
Copyright Holders
© 2020 The Authors.
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isVersionOf https://doi.org/10.1111/pim.12804
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https://creativecommons.org/licenses/by/4.0/