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Defining In Vivo Transcription Factor Complexes of the Murine CD21 and CD23 Genes¹

Division of Cell Biology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84112

The expression of the CD21 and CD23 genes is coincident with differentiation from transition 1 B cells (T1) to transition 2 B cells (T2). To define constituents controlling CD21 and CD23 expression, we conducted chromatin immunoprecipitation analyses for candidate transcription factors. We found constitutive binding of Oct-1, NFAT species, YY1, NF-B-p52, Pax5, E2A, and RBP-J to CD21 sequences and NF-B-p52, Pax5, NFAT species, E2A, and RBP-J to CD23 promoter sequences. Splenic T and B cell subsets displayed constitutive binding of YY1, NF-B-p52, Pax5, and Oct-1 proteins to CD21 sequences in B cells but no specific binding of NFATc3 or Pax5 in T cells. Similarly, CD23 sequences demonstrated constitutive binding of NF-B-p52 in splenic T and B cells but only Pax5 in B cells. Of the various NFAT species, only a subset were found forming constitutive DNA/protein complexes with the CD21, CD23, and IL-2 gene sequences. Maturing B cells in the marrow possess stable Pax5 complexes on CD19, CD21, and CD23 gene promoters in the nuclei of such cells, even though only CD19 is expressed. The similarity of genetic controlling elements between the CD21 and CD23 genes does not suggest a mechanism for alternative regulation of these genes; however, separation of splenic B cell subsets into T1, T2, marginal zone (MZ), and mature follicular B cells, followed by quantitative RT-PCR, demonstrated the lack of appreciable CD23 transcripts in CD21⁺ MZ cells. We propose an alternative derivation of MZ cells as maturing directly from T1 cells, leaving CD23 transcriptionally inactive in that lineage of cells.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This research was funded, in part, by National Institutes of Health Grant R01 AI2458 (to J.H.W.) and National Institutes of Health Grants R01 AI-32223 and AR-43521 (to J.J.W.).

² Address correspondence and reprint requests to Dr. John H. Weis, Department of Pathology, University of Utah School of Medicine, 15 North Medical Drive East, Salt Lake City, UT 84112. E-mail address: john.weis{at}path.utah.edu

³ Abbreviations used in this paper: T1, transition 1 B cell; BAFF, B cell-activating factor; ChIP, chromatin immunoprecipitation; CsA, cyclosporine; FM, follicular mature; F-OH, formaldehyde; MZ, marginal zone; NIDO, nidogen; RIPA, radioimmunoprecipitation assay; T2, transition 2 B cell.