Marcia A. ChanNicole M. GigliottiPonpan MatangkasombutStephen B. GauldJohn C. CambierLanny J. RosenwasserChildren's Mercy Hospitals and ClinicsMahidol UniversityHarvard School of Public HealthChildren's Research InstituteMedical College of WisconsinNational Jewish Health2018-09-242018-09-242010-12-01Clinical Immunology. Vol.137, No.3 (2010), 330-33615217035152166162-s2.0-78149285064https://repository.li.mahidol.ac.th/handle/20.500.14594/29168CD23 is the low affinity receptor for IgE and in B cells CD23 has been proposed to play a role in the regulation of IgE synthesis. CD23 is expressed also on other cell types including monocytes/macrophages, eosinophils, follicular dendritic cells and intestinal epithelial cells none of which is capable of expressing IgE. The diverse nature of the expressing cells suggests that either the CD23-mediated signal transduction pathway may be different among the cell types or biological outcomes differ in different cells in response to the same signaling pathway. To address this issue, the CD23 signaling pathway was analyzed and compared in primary tonsillar B cells and in the monocytic cell lines U937 and THP-1. Activation of the tyrosine kinase Fyn and the serine/threonine kinase Akt were only observed in B cells. These results suggest that the CD23-mediated signal transduction pathways in human B cells and human monocytes are different. © 2010 Elsevier Inc.Mahidol UniversityImmunology and MicrobiologyMedicineArticleSCOPUS10.1016/j.clim.2010.08.005