Evidence map›Paper›PMID 17983655›Full record

ArticleMolecular immunology2008

Activation-induced deaminase-mediated class switch recombination is blocked by anti-IgM signaling in a phosphatidylinositol 3-kinase-dependent fashion.

Lynn M Heltemes-Harris, Patricia J Gearhart, Paritosh Ghosh, Dan L Longo

Open access · greenAbstract read
In one paragraph

Article in Molecular immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Oxaliplatin Treatment Alters Systemic Immune Responses.BioMed research international · 2019
    Article
  7. Article
  8. Article
  9. ATAD5 deficiency decreases B cell division and Igh recombination.Journal of immunology (Baltimore, Md. : 1950) · 2015
    Article
  10. IgH chain class switch recombination: mechanism and regulation.Journal of immunology (Baltimore, Md. : 1950) · 2014
    Review
  11. Article
  12. Article
  13. AID and somatic hypermutation.Advances in immunology · 2010
    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

4 authors at 2 institutions in 1 country.

Lynn M Heltemes-HarrisLaboratory of Immunology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Patricia J Gearhart
Paritosh Ghosh
Dan L Longo
National Institutes of Health · USNational Institute on Aging · US

Funding

Protein Interactions in Antibody DiversityZ01AG000732 · NIA · NATIONAL INSTITUTE ON AGING · PI GEARHART, PATRICIA J · 1996 to 2008
$974k
Shaping The Preimmune B Cell RepertoireZ01AG000164 · NIA · NATIONAL INSTITUTE ON AGING · PI LONGO, DAN L. · 2002 to 2008
$462k
Roles for Transcription in Antibody DiversityZ01AG000714 · NIA · NATIONAL INSTITUTE ON AGING · PI GEARHART, PATRICIA J · 1988 to 2008
$319k
Intramural NIH HHS Z01 AG000164Intramural NIH HHS Z01 AG000732
6 · The paper itself

Abstract

Activation-induced deaminase (AID) is expressed in activated B lymphocytes and initiates somatic hypermutation and class switch recombination. To determine if different stimuli affect the expression and function of AID, we monitored AID activity in murine B cells stimulated ex vivo with various ligands. AID was rapidly expressed at both the RNA and protein levels following stimulation with LPS, LPS plus IL-4, and anti-CD40 plus IL-4, but was delayed after stimulation with anti-IgM plus IL-4. By day 4, AID was expressed in all groups; however, cells stimulated with anti-IgM plus IL-4 did not undergo switch recombination. These cells expressed normal levels of gamma 1 germline transcripts, implying that the gamma 1 switch region was accessible. Furthermore, switching was suppressed by the addition of anti-IgM to cells stimulated with LPS plus IL-4 or anti-CD40 plus IL-4, even though AID was expressed. The lack of class switch recombination could be reversed by inhibition of phosphatidylinositol 3-kinase (PI3K). This suggests that activation through the B cell receptor induces PI3K, which interferes with the function of AID.

Indexed as

Immunoglobulin Class SwitchingAICDA (Activation-Induced Cytidine Deaminase)AnimalsB-LymphocytesCD40 AntigensCell DifferentiationCytidine DeaminaseImmunoglobulin MMiceMice, Inbred BALB CPhosphatidylinositol 3-KinasesReceptors, Antigen, B-CellSignal TransductionSomatic Hypermutation, ImmunoglobulinToll-Like ReceptorsAICDA (Activation-Induced Cytidine Deaminase)CD40 AntigensCytidine DeaminaseImmunoglobulin MPhosphatidylinositol 3-KinasesReceptors, Antigen, B-CellToll-Like Receptors

Identifiers

PMID17983655
PMCPMC2274886
OpenAlexW1966498244

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.