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• W2157725749 abstract "To identify changes in the regulation of B cell receptor (BCR) signals during the development of human B cells, we generated genome-wide gene expression profiles using the serial analysis of gene expression (SAGE) technique for CD34+ hematopoietic stem cells (HSCs), pre-B cells, naive, germinal center (GC), and memory B cells. Comparing these SAGE profiles, genes encoding positive regulators of BCR signaling were expressed at consistently lower levels in naive B cells than in all other B cell subsets. Conversely, a large group of inhibitory signaling molecules, mostly belonging to the immunoglobulin superfamily (IgSF), were specifically or predominantly expressed in naive B cells. The quantitative differences observed by SAGE were corroborated by semiquantitative reverse transcription–polymerase chain reaction (RT-PCR) and flow cytometry. In a functional assay, we show that down-regulation of inhibitory IgSF receptors and increased responsiveness to BCR stimulation in memory as compared with naive B cells at least partly results from interleukin (IL)-4 receptor signaling. Conversely, activation or impairment of the inhibitory IgSF receptor LIRB1 affected BCR-dependent Ca2+ mobilization only in naive but not memory B cells. Thus, LIRB1 and IL-4 may represent components of two nonoverlapping gene expression programs in naive and memory B cells, respectively: in naive B cells, a large group of inhibitory IgSF receptors can elevate the BCR signaling threshold to prevent these cells from premature activation and clonal expansion before GC-dependent affinity maturation. In memory B cells, facilitated responsiveness upon reencounter of the immunizing antigen may result from amplification of BCR signals at virtually all levels of signal transduction." @default.
• W2157725749 created "2016-06-24" @default.
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• W2157725749 date "2002-11-18" @default.
• W2157725749 modified "2023-09-24" @default.
• W2157725749 title "Silencing of B Cell Receptor Signals in Human Naive B Cells" @default.
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• W2157725749 doi "https://doi.org/10.1084/jem.20020881" @default.
• W2157725749 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2193982" @default.
• W2157725749 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12438421" @default.
• W2157725749 hasPublicationYear "2002" @default.
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