Evidence map›Paper›PMID 16801401›Full record

ArticleThe Journal of experimental medicine2006

Essential role of membrane cholesterol in accelerated BCR internalization and uncoupling from NF-kappa B in B cell clonal anergy.

Mathieu Bléry, Lina Tze, Lisa A Miosge, Jesse E Jun, Christopher C Goodnow

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

29 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Sterols and immune mechanisms in asthma.The Journal of allergy and clinical immunology · 2023
    Review
  8. Article
  9. The Ins and Outs of Antigen Uptake in B cells.Frontiers in immunology · 2022
    Review
  10. Review
  11. Review
  12. Article
  13. Haematologica · 2018
    Article
  14. Article
  15. Article
  16. Review
  17. Tolerant anti-insulin B cells are effective APCs.Journal of immunology (Baltimore, Md. : 1950) · 2013
    Article
  18. Encounter with antigen-specific primed CD4 T cells promotes MHC class II degradation in dendritic cells.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Mathieu BléryJohn Curtin School of Medical Research, The Australian National University, Canberra ACT 2601, Australia.
Lina Tze
Lisa A Miosge
Jesse E Jun
Christopher C Goodnow
Australian National University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Divergent hypotheses exist to explain how signaling by the B cell receptor (BCR) is initiated after antigen binding and how it is qualitatively altered in anergic B cells to selectively uncouple from nuclear factor kappaB and c-Jun N-terminal kinase pathways while continuing to activate extracellular signal-regulated kinase and calcium-nuclear factor of activated T cell pathways. Here we find that BCRs on anergic cells are endocytosed at a very enhanced rate upon binding antigen, resulting in a large steady-state pool of intracellularly sequestered receptors that appear to be continuously cycling between surface and intracellular compartments. This endocytic mechanism is exquisitely sensitive to the lowering of plasma membrane cholesterol by methyl-beta-cyclodextrin, and, when blocked in this way, the sequestered BCRs return to the cell surface and RelA nuclear accumulation is stimulated. In contrast, when plasma membrane cholesterol is lowered and GM1 sphingolipid markers of membrane rafts are depleted in naive B cells, this does not diminish BCR signaling to calcium or RelA. These results provide a possible explanation for the signaling changes in clonal anergy and indicate that a chief function of membrane cholesterol in B cells is not to initiate BCR signaling, but instead to terminate a subset of signals by rapid receptor internalization.

Indexed as

AnimalsB-LymphocytesCholesterolClonal AnergyMembrane LipidsMiceMice, Inbred C57BLMice, TransgenicNF-kappa BReceptors, Antigen, B-CellSignal TransductionCholesterolMembrane LipidsNF-kappa BReceptors, Antigen, B-Cell

Identifiers

PMID16801401
PMCPMC2118358
OpenAlexW2106474854

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.