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and Ets Protein Family Members Regulate the Human Myeloid IgA Fc Receptor (FcR, CD89) Promoter1
Allergy Research Center and Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan; CREST, Japan Science and Technology Corp., Kawaguchi City, Japan; and Department of Molecular Cell Immunology and Allergology, Advanced Medical Research Center, Nihon University School of Medicine, Tokyo, Japan
Fc
R (CD89), the FcR for IgA, is expressed exclusively in myeloid cells, including monocytes/macrophages, neutrophils, and eosinophils, and is thought to mediate IgA-triggered cellular functions in immunity. Here we demonstrate that the FcR 5'-flanking region from -102 to -64 relative to the ATG translation initiation codon is essential for promoter activity and contains two functional binding motifs for C/EBP and Ets family members at -74 and -92, respectively. EMSAs and cotransfection experiments show that C/EBP acts as a major activator of the FcR promoter at least in immature myeloid cells. In addition, we found two additional functional targets of C/EBP at -139 and -127. On the other hand, the FcR Ets binding motif could bind Elf-1 and mediate the trans-activation by cotransfected Elf-1, but a major component of the complex forming on this site appears to be an unidentified Ets-like nuclear protein that is preferentially detected in cells of hemopoietic origin. Furthermore, separation of the C/EBP and Ets binding sites reduces FcR promoter activity, suggesting some functional interaction between these factors. As the in vivo role of FcR is still incompletely defined, these findings reveal the features controlling the FcR promoter in myeloid lineage and provide a foundation for clarifying regulatory mechanisms of FcR gene expression associated with its potential roles.
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