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J Immunol. 2019 Aug 15;203(4):813-824. doi: 10.4049/jimmunol.1801156. Epub 2019 Jul 3.

Cutaneous Exposure to Clinically Relevant Lone Star Ticks Promotes IgE Production and Hypersensitivity through CD4+ T Cell- and MyD88-Dependent Pathways in Mice.

Author information

1
Beirne B. Carter Center for Immunology Research, University of Virginia School of Medicine, Charlottesville, VA 22908.
2
Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, VA 22908; and.
3
Department of Pathology, University of Virginia School of Medicine, Charlottesville, VA 22908.
4
Beirne B. Carter Center for Immunology Research, University of Virginia School of Medicine, Charlottesville, VA 22908; loren@virginia.edu.

Abstract

Tick-borne allergies are a growing public health concern and have been associated with the induction of IgE-mediated food allergy to red meat. However, despite the increasing prevalence of tick bite-induced allergies, the mechanisms by which cutaneous exposure to ticks leads to sensitization and the production of IgE Abs are poorly understood. To address this question, an in vivo approach was used to characterize the IgE response to lone star tick proteins administered through the skin of mice. The results demonstrated that tick sensitization and challenge induced a robust production of IgE Abs and supported a role for IgE-mediated hypersensitivity reactions in sensitized animals following oral administration of meat. The induction of IgE responses was dependent on cognate CD4+ T cell help during both the sensitization phase and challenge phase with cutaneous tick exposure. In addition, IgE production was dependent on B cell-intrinsic MyD88 expression, suggesting an important role for TLR signaling in B cells to induce IgE responses to tick proteins. This model of tick-induced IgE responses could be used to study the factors within tick bites that cause allergies and to investigate how sensitization to food Ags occurs through the skin that leads to IgE production.

PMID:
31270149
PMCID:
PMC6684363
[Available on 2020-08-15]
DOI:
10.4049/jimmunol.1801156

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