Selective ablation of basophils in mice reveals their nonredundant role in acquired immunity against ticks.
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.
Wada
Takeshi
T
Department of Immune Regulation, Tokyo Medical and Dental University Graduate School, Tokyo, Japan.
Ishiwata
Kenji
K
Koseki
Haruhiko
H
Ishikura
Tomoyuki
T
Ugajin
Tsukasa
T
Ohnuma
Naotsugu
N
Obata
Kazushige
K
Ishikawa
Ryosuke
R
Yoshikawa
Soichiro
S
Mukai
Kaori
K
Kawano
Yohei
Y
Minegishi
Yoshiyuki
Y
Yokozeki
Hiroo
H
Watanabe
Naohiro
N
Karasuyama
Hajime
H
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
D017455:Receptors, IgE; D007073:Immunoglobulin E; C512639:Mcpt8 protein, mouse; D053802:Tryptases