Evidence map›Paper›PMID 12438421›Full record

ArticleThe Journal of experimental medicine2002

Silencing of B cell receptor signals in human naive B cells.

Niklas Feldhahn, Ines Schwering, Sanggyu Lee, Maria Wartenberg, Florian Klein, Hui Wang, Guolin Zhou, San Ming Wang, Janet D Rowley, Jürgen Hescheler and 4 more

RetractedOpen access · bronzeAbstract readRetracted Publication
In one paragraph

Article in The Journal of experimental medicine, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.6field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Src-like adaptor protein (SLAP) regulates B cell receptor levels in a c-Cbl-dependent manner.Proceedings of the National Academy of Sciences of the United States of America · 2006
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Deficiency of Bruton's tyrosine kinase in B cell precursor leukemia cells.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
  10. Article
  11. Defective B cell responses in the absence of SH2D1A.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
  12. Article
  13. Article
  14. T lymphoid differentiation in human bone marrow.Proceedings of the National Academy of Sciences of the United States of America · 2003
    Article
  15. Transcriptional analysis of the B cell germinal center reaction.Proceedings of the National Academy of Sciences of the United States of America · 2003
    Article
4 · The record

Corrections and comments

  • Retraction · 2006-11-27Concerns/Issues about Data · Concerns/Issues about Results and/or Conclusions · Error in Data · Error in Results and/or Conclusions · Unreliable Data · Unreliable Results and/or Conclusions ·
  • Retracted
5 · Who and what money

Authors and funding

14 authors at 4 institutions in 2 countries.

Niklas FeldhahnInstitute for Medical Microbiology, Immunology and Hygiene, University of Cologne, 50931 Köln, Germany.
Ines Schwering
Sanggyu Lee
Maria Wartenberg
Florian Klein
Hui Wang
Guolin Zhou
San Ming Wang
Janet D Rowley
Jürgen Hescheler
Martin Krönke
Klaus Rajewsky
Ralf Küppers
Markus Müschen
University of Cologne · DEInstitute of Medical Microbiology and Hygiene · DEUniversity of Chicago · USHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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 Ca(2+) 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.

Indexed as

Antigens, CD34B-LymphocytesGene Expression ProfilingHumansReceptors, Antigen, B-CellReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSignal TransductionAntigens, CD34Receptors, Antigen, B-CellRNA, Messenger

Identifiers

PMID12438421
PMCPMC2193982
OpenAlexW2157725749

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.