Johal KJ, Chichester KL, Oliver ET, et al. - Since the mechanisms underlying disease pathogenesis in chronic spontaneous urticaria (CSU) and improvement with omalizumab, a monoclonal IgG anti-human IgE antibody, are unknown, researchers sought to examine if the rate of clinical remission is concordant with baseline basophil features or the rate of change of IgE-dependent functions of basophils and/or plasmacytoid dendritic cells during omalizumab therapy. Adults (n = 18) with refractory CSU were given omalizumab 300 mg once a month for 90 days. At baseline, patients were classified as CSU-responder (CSU-R) or CSU-non-responder (CSU-NR), as well as basopenic (B) or non-basopenic (NB) based on basophil functional phenotypes, determined by in vitro histamine release (HR) responses to anti-IgE antibody. CSU-R/NB individuals showed the most rapid and complete symptom improvement. Changes in basophil IgE based HR, surface IgE or FcεRI are not related to kinetics in the change in clinical symptoms. HR-determined baseline basophil count and basophil functional phenotype may be predictive of omalizumab responsiveness.