Evidence map›Paper›PMID 9200459›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)1997

B cell antigen receptor desensitization: disruption of receptor coupling to tyrosine kinase activation.

B J Vilen, S J Famiglietti, A M Carbone, B K Kay, J C Cambier

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Article
  2. Review
  3. Heterogeneity of B Cell Functions in Stroke-Related Risk, Prevention, Injury, and Repair.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016
    Review
  4. Anti-CD79 antibody induces B cell anergy that protects against autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2014
    Article
  5. Article
  6. Article
  7. Article
  8. Endocytic sequestration of the B cell antigen receptor and toll-like receptor 9 in anergic cells.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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.

B J VilenDepartment of Pediatrics, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO 80206, USA.
S J Famiglietti
A M Carbone
B K Kay
J C Cambier

Funding

THE REGULATION OF V ALPHA 7 EXPRESSING T CELLSP01AI022295 · NIAID · NATIONAL JEWISH HEALTH · PI PELANDA, ROBERTA · 1985 to 2011
$11.7M
BIOLOGICAL FUNCTION OF B CELL RECEPTOR DESTABILIZATIONK22AI001756 · NIAID · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI VILEN, BARBARA J · 2001 to 2002
$269k
SIGNAL TRANSDUCTION IN B CELL ACTIVATIONR01AI021768 · NIAID · NATIONAL JEWISH HEALTH · PI CAMBIER, JOHN C. · 1985 to 1995
–
NIAID NIH HHS AI21768NIAID NIH HHS AI22295NIAID NIH HHS K22 AI001756NIAID NIH HHS P01 AI022295
6 · The paper itself

Abstract

Antigen binding to the B cell receptor (BCR) induces receptor desensitization, a condition characterized by cellular unresponsiveness to subsequent Ag stimulation despite the continued ability to bind Ag. To better understand the molecular mechanism of this unresponsiveness, we have used complementary lymphoma (K46 mu) and Ig transgenic (3-83 mu delta) mouse models to study regulation of BCR signaling. Our findings in the lymphoma model show that an initial Ag encounter renders receptors unresponsive to subsequent Ag challenge, as measured by their inability to mobilize Ca2+ and to mediate phosphorylation of receptor-proximal kinases, including Lyn, Blk, and Syk. Most importantly, the Ig alpha and Ig beta components of desensitized receptors are not phosphorylated, and receptor-associated kinases are not activated upon Ag challenge. The molecular defect does not appear to result from Lyn inactivation, sequestration, or repression, since Lyn from desensitized cell lysates is activated in vitro by synthetic doubly phosphorylated immunoreceptor tyrosine-based activation motif peptides. A similar deficit in Ag-induced receptor phosphorylation was observed in desensitized B cells from 3-83 mu delta transgenic mice. These studies indicate that Ag receptor desensitization reflects an inability to initiate activation of receptor-associated kinases that normally phosphorylate receptor Ig alphabeta subunits, leading to signal propagation.

Indexed as

AnimalsAntigensB-LymphocytesHumansLigandsLymphomaMiceMice, TransgenicProtein-Tyrosine KinasesReceptors, Antigen, B-CellSignal TransductionTumor Cells, CulturedAntigensLigandsProtein-Tyrosine KinasesReceptors, Antigen, B-Cell

Identifiers

PMID9200459
PMCPMC3931421

What OpenQuestion holds

Textmetadata
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.