Evidence map›Paper›PMID 29681901›Full record

ReviewFrontiers in immunology2018

Putting on the Brakes: Regulatory Kinases and Phosphatases Maintaining B Cell Anergy.

S Elizabeth Franks, John C Cambier

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Article
  3. A viral glycoprotein targets IgGEMBO molecular medicine · 2026
    Article
  4. Review
  5. Posttranscriptional control of the B cell receptor by HuR is essential for innate B cell maintenance and function.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. SARS-CoV-2 infection relaxes peripheral B cell tolerance.The Journal of experimental medicine · 2022
    Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review
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

2 authors at 1 institution in 1 country.

S Elizabeth FranksDepartment of Immunology and Microbiology, University of Colorado Denver School of Medicine, Aurora, CO, United States.
John C CambierDepartment of Immunology and Microbiology, University of Colorado Denver School of Medicine, Aurora, CO, United States.
University of Colorado Denver · US

Funding

Autoimmunity risk alleles compromising B cell anergyR01AI124487 · NIAID · UNIVERSITY OF COLORADO DENVER · PI CAMBIER, JOHN C · 2016 to 2020
$2.5M
B Cells and Type 1 DiabetesR01DK096492 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI CAMBIER, JOHN C · 2012 to 2016
$1.6M
Perturbation of B cell anergy in T1DR21AI124488 · NIAID · UNIVERSITY OF COLORADO DENVER · PI CAMBIER, JOHN C · 2016 to 2017
$428k
NIAID NIH HHS R01 AI124487NIAID NIH HHS R21 AI124488NIDDK NIH HHS R01 DK096492
6 · The paper itself

Abstract

B cell antigen receptor (BCR) signaling is a tightly regulated process governed by both positive and negative mediators/regulators to ensure appropriate responses to exogenous and autologous antigens. Upon naïve B cell recognition of antigen CD79 [the immunoreceptor tyrosine-based activation motif (ITAM)-containing signaling subunit of the BCR] is phosphorylated and recruits Src and Syk family kinases that then phosphorylate proximal intermediaries linked to downstream activating signaling circuitry. This plasma membrane localized signalosome activates PI3K leading to generation of PIP3 critical for membrane localization and activation of plecktrin homology domain-containing effectors. Conversely, in anergic B cells, chronic antigen stimulation drives biased monophosphorylation of CD79 ITAMs leading to recruitment of Lyn, but not Syk, which docks only to bi-phosphorylated ITAMS. In this context, Lyn appears to function primarily as a driver of inhibitory signaling pathways promoting the inhibition of the PI3K pathway by inositol phosphatases, SHIP-1 and PTEN, which hydrolyze PIP3 to PIP2. Lyn may also exert negative regulation of signaling through recruitment of SHP-1, a tyrosine phosphatase that dephosphorylates activating signaling molecules. Alleles of genes that encode or regulate expression of components of this axis, including SHIP-1, SHP-1, Csk/PTPn22, and Lyn, have been shown to confer risk of autoimmunity. This review will discuss functional interplay of components of this pathway and the impact of risk alleles on its function.

Indexed as

AnimalsB-LymphocytesClonal AnergyHumansPhosphoric Monoester HydrolasesProtein KinasesReceptors, Antigen, B-CellPhosphoric Monoester HydrolasesProtein KinasesReceptors, Antigen, B-CellanergyB cellskinaseslynphosphatasesPtenSHIP-1SHP-1

Identifiers

PMID29681901
PMCPMC5897502
OpenAlexW2805720509

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.