Analysis of the major patterns of B cell gene expression changes in response to short-term stimulation with 33 single ligands.

TitleAnalysis of the major patterns of B cell gene expression changes in response to short-term stimulation with 33 single ligands.
Publication TypeJournal Article
Year of Publication2004
AuthorsZhu X, Hart R, Chang M S, Kim J-W, Lee S Y, Cao Y A, Mock D, Ke E, Saunders B, Alexander A, Grossoehme J, Lin K-M, Yan Z, Hsueh R, Lee J, Scheuermann RH, Fruman DA, Seaman W, Subramaniam S, Sternweis P, Simon MI, Choi S
JournalJ Immunol
Volume173
Issue12
Pagination7141-9
Date Published2004 Dec 15
ISSN0022-1767
KeywordsAnimals, Antibodies, Anti-Idiotypic, B-Lymphocyte Subsets, CD40 Ligand, Cell Proliferation, Cells, Cultured, CpG Islands, Gene Expression Profiling, Gene Expression Regulation, Interleukin-4, Ligands, Lipopolysaccharides, Lymphocyte Activation, Male, Mice, Mice, Inbred C57BL, Oligonucleotide Array Sequence Analysis, Polymerase Chain Reaction, Spleen, Up-Regulation
Abstract

We examined the major patterns of changes in gene expression in mouse splenic B cells in response to stimulation with 33 single ligands for 0.5, 1, 2, and 4 h. We found that ligands known to directly induce or costimulate proliferation, namely, anti-IgM (anti-Ig), anti-CD40 (CD40L), LPS, and, to a lesser extent, IL-4 and CpG-oligodeoxynucleotide (CpG), induced significant expression changes in a large number of genes. The remaining 28 single ligands produced changes in relatively few genes, even though they elicited measurable elevations in intracellular Ca(2+) and cAMP concentration and/or protein phosphorylation, including cytokines, chemokines, and other ligands that interact with G protein-coupled receptors. A detailed comparison of gene expression responses to anti-Ig, CD40L, LPS, IL-4, and CpG indicates that while many genes had similar temporal patterns of change in expression in response to these ligands, subsets of genes showed unique expression patterns in response to IL-4, anti-Ig, and CD40L.

DOI10.4049/jimmunol.173.12.7141
PubMed URLhttp://www.ncbi.nlm.nih.gov/pubmed/15585835?dopt=Abstract
Alternate TitleJ. Immunol.
PubMed ID15585835