Interleukin-4 Signals Regulating CD23 Gene Expression in Human B Cells: Protein Kinase C-Independent Signaling Pathways

• Published in: Cellular immunology Vol. 146; no. 1; pp. 171 - 185
• Main Authors: Lee, Choong-Eun, Yoon, Suk-Ran, Pyun, Kwang-Ho
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 1993
• Subjects: B-Lymphocytes - drug effects; B-Lymphocytes - immunology; Cells, Cultured - drug effects; Diglycerides - pharmacology; Gene Expression Regulation - drug effects; Humans; Immunoglobulin E - immunology; Interleukin-4 - immunology; Palatine Tonsil - cytology; Phorbol Esters - pharmacology; Protein Kinase C; Protein-Tyrosine Kinases; Receptors, IgE - genetics; Signal Transduction; Transcriptional Activation
• ISSN: 0008-8749; 1090-2163
• DOI: 10.1006/cimm.1993.1015

Signal transduction by IL-4 leading to the activation of CD23(FcϵRII) gene expression using human tonsillar B cells was studied. IL-4 stimulated CD23 mRNA transcription within hours (1-4 hr) which preceded the later induction of cell surface CD23. The induction of CD23 gene transcription by IL-4 was not adversely affected by cycloheximide, suggesting that post-translational modifications are accounted for the gene activation. PKC activators (PMA, diacylglycerol, indolactam) were effective inducers of CD23 gene expression, whereas calcium ionophores were not. PMA and IL-4 also displayed similar induction kinetics for CD23 mRNA. However, the signaling pathways utilized by the two agents appear distinct as shown by (1) cotreatment of IL-4 and PMA caused CD23 gene expression over the maximum level inducible by each agent alone and (2) unlike the PMA-induced CD23 expression, the IL-4-induced expression was not affected by PKC inhibitors. These results strongly suggest that IL-4 signals leading to CD23 gene activation are mediated via a PKC-independent pathway. A possible role of tyrosine kinases in the regulation of CD23 expression is discussed.