Effects of anti-IgM suppression on polyclonally activated murine B cells: Analysis of immunoglobulin mRNA, gene specific nuclear factors and cell cycle distribution

Adriana Marcuzzi, Brian van Ness, Todd Rouse, David Lafrenz

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

Abstract

Polyclonal activation of murine B cells with bacterial lipo-polysaccharide (LPS) and dextran sulfate (DxS) results in cell proliferation as well as increased immunoglobulin gene transcription and antibody secretion. When added to B cell cultures during mitogen activation, anti-μ antibody suppresses the rate of proliferation and immunoglobulin gene expression. Using this model system we show that co-cultures of B cells with LPS/DxS and anti-μ resulted in a decrease of both μ and κ chain mRNA. Suppression did not prevent B cell entry into cycle nor a significant alteration in the distribution of cells in phases of cell cycle, although it did prolong the cycle transit time in a dose dependent fashion as determined by bromodeoxyuridine pulse labelling. Analysis of B cell specific nuclear binding factors, which previously have been shown to be important in regulating immunoglobulin gene transcription were examined. Results show that the kappa-specific enhancer binding activity of NF-κB was induced in activated as well as suppressed cultures. The lymphoid specific factor NF-A2, which recognizes the octamer sequence motif in the promoters of immunoglobulin genes, was induced by the polyclonal activation but was selectively lost in extracts from suppressed cells. Thus, specific regulation of the nuclear factor which plays a critical role in both heavy and light chain immunoglobulin gene expression may contribute to the transcriptional suppression observed in anti-μ treated B cells.

Original languageEnglish (US)
Pages (from-to)10455-10472
Number of pages18
JournalNucleic acids research
Volume17
Issue number24
DOIs
StatePublished - Dec 25 1989

Bibliographical note

Funding Information:
ACKNOWLEDGMENTS This work was supported by funds from the Medical Research Service, Department of Veterans Affairs (D.L.) and by grant GM 37687 from the National Institutes of Health (B.V.N.)

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