4.7 Article

Basophils and allergic inflammation

Journal

JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Volume 132, Issue 4, Pages 789-801

Publisher

MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2013.07.046

Keywords

Basophil; allergy; T(H)2 cytokine; thymic stromal lymphopoietin; allergic rhinitis; asthma; atopic dermatitis; urticaria; food allergy; eosinophilic esophagitis; IgE

Funding

  1. National Institutes of Health [AI061570, AI087990, AI074878, AI095776, AI102942, AI095466, AI095608, AI097333]
  2. Burroughs Wellcome Fund Investigator in Pathogenesis of Infectious Disease Award [KL2-RR024132, F32-AI085828]
  3. National Institutes of Health (NIH)

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Basophils were discovered by Paul Ehrlich in 1879 and represent the least abundant granulocyte population in mammals. The relative rarity of basophils and their phenotypic similarities with mast cells resulted in this cell lineage being historically overlooked, both clinically and experimentally. However, recent studies in human subjects and murine systems have shown that basophils perform nonredundant effector functions and significantly contribute to the development and progression of T(H)2 cytokine-mediated inflammation. Although the potential functions of murine and human basophils have provoked some controversy, recent genetic approaches indicate that basophils can migrate into lymphoid tissues and, in some circumstances, cooperate with other immune cells to promote optimal T(H)2 cytokine responses in vivo. This article provides a brief historical perspective on basophil-related research and discusses recent studies that have identified previously unappreciated molecules and pathways that regulate basophil development, activation, and function in the context of allergic inflammation. Furthermore, we highlight the unique effector functions of basophils and discuss their contributions to the development and pathogenesis of allergic inflammation in human disease. Finally, we discuss the therapeutic potential of targeting basophils in preventing or alleviating the development and progression of allergic inflammation.

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