Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 212, Issue 4, Pages 513-524Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20141671
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Funding
- A.P. Giannini Medical Research Foundation
- National Institutes of Health [AI095319, AI103146, AI026918, AI030663, AI119944]
- Howard Hughes Medical Institute
- University of California, San Francisco Sabre Center
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Vertebrate immunity has evolved a modular architecture in response to perturbations. Allergic inflammation represents such a module, with signature features of antigen-specific IgE and tissue eosinophilia, although the cellular and molecular circuitry coupling these responses remains unclear. Here, we use genetic and imaging approaches in models of IgE-dependent eosinophilic dermatitis to demonstrate a requisite role for basophils. After antigenic inflammation, basophils initiate transmigration like other granulocytes but, upon activation via their high-affinity IgE receptor, alter their migratory kinetics to persist at the endothelium. Prolonged basophil-endothelial interactions, in part dependent on activation of focal adhesion kinases, promote delivery of basophil-derived IL-4 to the endothelium and subsequent induction of endothelial vascular cell adhesion molecule-1 (VCAM-1), which is required for eosinophil accumulation. Thus, basophils are gatekeepers that link adaptive immunity with innate effector programs by altering access to tissue sites by activation-induced interactions with the endothelium.
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