Journal
ALLERGY
Volume 69, Issue 5, Pages 674-677Publisher
WILEY-BLACKWELL
DOI: 10.1111/all.12375
Keywords
allergy; basophil; asthma; IgE; omalizumab
Categories
Funding
- Stuart E. Starr Chair in Pediatrics
- Department of Defense [W81XWH-11-1-0507]
- Institute for Translational Medicine and Therapeutics [UL1-RR024134]
- National Institutes of Health [AI061570, AI087990, AI074878, AI083480, AI102 942, AI095466, AI095608, AI097333, AI106697, F32-AI085828, T32-AI060516, F32-AI098365]
- Burroughs Wellcome Fund
- NIH/NIDDK P30 Center for Molecular Studies in Digestive and Liver Diseases [P30-DK050306]
- Joint CHOP-Penn Center in Digestive, Liver and Pancreatic Medicine
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Basophils have been implicated in promoting the early development of T(H)2 cell responses in some murine models of T(H)2 cytokine-associated inflammation. However, the specific role of basophils in allergic asthma remains an active area of research. Recent studies in animal models and human subjects suggest that IgE may regulate the homeostasis of human basophil populations. Here, we examine basophil populations in children with severe asthma before and during therapy with the IgE-directed monoclonal antibody omalizumab. Omalizumab therapy was associated with a significant reduction in circulating basophil numbers, a finding that was concurrent with improved clinical outcomes. The observation that circulating basophils are reduced following omalizumab therapy supports a mechanistic link between IgE levels and circulating basophil populations, and may provide new insights into one mechanism by which omalizumab improves asthma symptoms.
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