Reduced FcεRI-Mediated Release of Asthma-Promoting Cytokines and Chemokines from Human Basophils during Omalizumab Therapy
Author(s) -
Janet M. Oliver,
Christy A. Tarleton,
Laura Gilmartin,
Tereassa Archibeque,
Clifford Qualls,
Lorena Diehl,
Bridget S. Wilson,
Mark Schuyler
Publication year - 2009
Publication title -
international archives of allergy and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.696
H-Index - 100
eISSN - 1423-0097
pISSN - 1018-2438
DOI - 10.1159/000250436
Subject(s) - omalizumab , basophil , histamine , immunoglobulin e , chemokine , medicine , immunology , cytokine , basal (medicine) , asthma , inflammation , antibody , insulin
Treating asthmatics with the humanized IgE-scavenging antibody, omalizumab (rhuMAb-E25, Xolair, reduces airways inflammation and asthma symptoms. Previously, omalizumab was shown to cause a dramatic and reversible loss of cell surface high-affinity IgE receptors, FcepsilonRI, from the peripheral blood basophils of asthmatics. The consequences of receptor loss for the FcepsilonRI-mediated synthesis and release of cytokines implicated in allergic asthma have not been examined.
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