title: Selective ablation of basophils in mice reveals their nonredundant role in acquired immunity against ticks.
abstract: Ticks are ectoparasitic arthropods that can transmit a variety of microorganisms to humans and animals during blood feeding, causing serious infectious disorders, including Lyme disease. Acaricides are pharmacologic agents that kill ticks. The emergence of acaricide-resistant ticks calls for alternative control strategies for ticks and tick-borne diseases. Many animals develop resistance to ticks after repeated infestations, but the nature of this acquired anti-tick immunity remains poorly understood. Here we investigated the cellular and molecular mechanisms underlying acquired resistance to Haemaphysalis longicornis ticks in mice and found that antibodies were required, as was IgFc receptor expression on basophils but not on mast cells. The infiltration of basophils at tick-feeding sites occurred during the second, but not the first, tick infestation. To assess the requirement for basophil infiltration to acquired tick resistance, mice expressing the human diphtheria toxin receptor under the control of the mast cell protease 8 (Mcpt8) promoter were generated. Diphtheria toxin administration to these mice selectively ablated basophils. Diphtheria toxin-mediated basophil depletion before the second tick infestation resulted in loss of acquired tick resistance. These data provide the first clear evidence, to our knowledge, that basophils play an essential and nonredundant role in antibody-mediated acquired immunity against ticks, which may suggest new strategies for controlling tick-borne diseases.
authors.affiliation: Department of Immune Regulation, Tokyo Medical and Dental University Graduate School, Tokyo, Japan.
authors.forename: Takeshi
authors.initials: T
authors.lastname: Wada
authors.forename: Kenji
authors.initials: K
authors.lastname: Ishiwata
authors.forename: Haruhiko
authors.initials: H
authors.lastname: Koseki
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Ishikura
authors.forename: Tsukasa
authors.initials: T
authors.lastname: Ugajin
authors.forename: Naotsugu
authors.initials: N
authors.lastname: Ohnuma
authors.forename: Kazushige
authors.initials: K
authors.lastname: Obata
authors.forename: Ryosuke
authors.initials: R
authors.lastname: Ishikawa
authors.forename: Soichiro
authors.initials: S
authors.lastname: Yoshikawa
authors.forename: Kaori
authors.initials: K
authors.lastname: Mukai
authors.forename: Yohei
authors.initials: Y
authors.lastname: Kawano
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Minegishi
authors.forename: Hiroo
authors.initials: H
authors.lastname: Yokozeki
authors.forename: Naohiro
authors.initials: N
authors.lastname: Watanabe
authors.forename: Hajime
authors.initials: H
authors.lastname: Karasuyama
mesh_terms: D000818:Animals; D001491:Basophils / Q000502:physiology*; D007073:Immunoglobulin E / Q000097:blood; D008407:Mast Cells / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D017455:Receptors, IgE / Q000502:physiology; D013984:Tick Infestations / Q000276:immunology*; D053802:Tryptases / Q000502:physiology
chemical_list: D017455:Receptors, IgE; D007073:Immunoglobulin E; C512639:Mcpt8 protein, mouse; D053802:Tryptases