Evidence map›Paper›PMID 30904131›Full record

ReviewAdvances in immunology2019

Signaling control of antibody isotype switching.

Zhangguo Chen, Jing H Wang

Open access · greenAbstract readReview
In one paragraph

Review in Advances in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Hepatitis C virus modified sE2Journal of virology · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Anti-Microorganisms · 2022
    Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. 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

2 authors at 1 institution in 1 country.

Zhangguo ChenDepartment of Immunology and Microbiology, University of Colorado Anschutz Medical Campus, Aurora, CO, United States. Electronic address: zhangguo.chen@ucdenver.edu.
Jing H WangDepartment of Immunology and Microbiology, University of Colorado Anschutz Medical Campus, Aurora, CO, United States. Electronic address: jing.wang@ucdenver.edu.
University of Colorado Anschutz Medical Campus · US

Funding

Elucidating Mechanism of Immune Evasion in Head and Neck CancersR01DE027329 · NIDCR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WANG, JING HONG, WANG, XIAO-JING · 2018 to 2022
$2.8M
A Novel Approach to Evaluate Genetic Variants in Primary Antibody DeficiencyR21AI133110 · NIAID · UNIVERSITY OF COLORADO DENVER · PI WANG, JING HONG · 2018 to 2019
$428k
NIAID NIH HHS R21 AI133110NIDCR NIH HHS R01 DE027329
6 · The paper itself

Abstract

Class switch recombination (CSR) generates isotype-switched antibodies with distinct effector functions essential for mediating effective humoral immunity. CSR is catalyzed by activation-induced deaminase (AID) that initiates DNA lesions in the evolutionarily conserved switch (S) regions at the immunoglobulin heavy chain (Igh) locus. AID-initiated DNA lesions are subsequently converted into DNA double stranded breaks (DSBs) in the S regions of Igh locus, repaired by non-homologous end-joining to effect CSR in mammalian B lymphocytes. While molecular mechanisms of CSR are well characterized, it remains less well understood how upstream signaling pathways regulate AID expression and CSR. B lymphocytes express multiple receptors including the B cell antigen receptor (BCR) and co-receptors (e.g., CD40). These receptors may share common signaling pathways or may use distinct signaling elements to regulate CSR. Here, we discuss how signals emanating from different receptors positively or negatively regulate AID expression and CSR.

Indexed as

AICDA (Activation-Induced Cytidine Deaminase)AnimalsB-Cell Activation Factor ReceptorB-LymphocytesCytidine DeaminaseDNA Breaks, Double-StrandedHumansImmunity, HumoralImmunoglobulin Class SwitchingImmunoglobulin Heavy ChainsImmunoglobulin IsotypesMiceReceptors, Antigen, B-CellRecombination, GeneticSignal TransductionToll-Like ReceptorsAICDA (Activation-Induced Cytidine Deaminase)B-Cell Activation Factor ReceptorCytidine DeaminaseImmunoglobulin Heavy ChainsImmunoglobulin IsotypesReceptors, Antigen, B-CellTNFRSF13C protein, humanToll-Like ReceptorsTransmembrane Activator and CAML Interactor ProteinActivation-induced deaminaseB cell antigen receptorCD40Class switch recombinationPI3KPTENSignal transductionToll-like receptor

Identifiers

PMID30904131
PMCPMC7875453
OpenAlexW2913112905

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.