Evidence map›Paper›PMID 18285461›Full record

ArticleMolecular and cellular biology2008

A role for interferon regulatory factor 4 in receptor editing.

Simanta Pathak, Shibin Ma, Long Trinh, Runqing Lu

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2008. 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
1.3field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Mechanisms of central tolerance for B cells.Nature reviews. Immunology · 2017
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Critical role of IRF-5 in regulation of B-cell differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  15. NF-kappaB activity marks cells engaged in receptor editing.The Journal of experimental medicine · 2009
    Article
  16. IRF4: Immunity. Malignancy! Therapy?Clinical cancer research : an official journal of the American Association for Cancer Research · 2009
    Review
  17. 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 1 institution in 1 country.

Simanta PathakDepartment of Genetics, Cell Biology, and Anatomy, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Shibin Ma
Long Trinh
Runqing Lu
University of Nebraska Medical Center · US

Funding

UNMC/EPPLEY CANCER CENTER SUPPORT GRANTP30CA036727 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Apar Kishor Ganti · 1985 to 2026
$55.0M
Molecular basis of the requirements for IRF4 and IRF8 in pre-B cell developmentR01AI067891 · NIAID · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI LU, RUNQING · 2006 to 2010
$1.8M
NCI NIH HHS P30 CA036727NIAID NIH HHS R01 AI067891
6 · The paper itself

Abstract

Receptor editing is the primary means through which B cells revise antigen receptors and maintain central tolerance. Previous studies have demonstrated that interferon regulatory factor 4 (IRF-4) and IRF-8 promote immunoglobulin light-chain rearrangement and transcription at the pre-B stage. Here, the roles of IRF-4 and -8 in receptor editing were analyzed. Our results show that secondary rearrangement was impaired in IRF-4 but not IRF-8 mutant mice, suggesting that receptor editing is defective in the absence of IRF-4. The role of IRF-4 in receptor editing was further examined in B-cell-receptor (BCR) transgenic mice. Our results show that secondary rearrangement triggered by membrane-bound antigen was defective in the IRF-4-deficient mice. Our results further reveal that the defect in secondary rearrangement is more severe at the immunoglobulin lambda locus than at the kappa locus, indicating that IRF-4 is more critical for the lambda rearrangement. We provide evidence demonstrating that the expression of IRF-4 in immature B cells is rapidly induced by self-antigen and that the reconstitution of IRF-4 expression in the IRF-4 mutant immature B cells promotes secondary rearrangement. Thus, our studies identify IRF-4 as a nuclear effector of a BCR signaling pathway that promotes secondary rearrangement at the immature B-cell stage.

Indexed as

AnimalsAutoantigensB-LymphocytesCell DifferentiationCell MembraneCell ProliferationCells, CulturedImmunoglobulinsInterferon Regulatory Factor-4Interferon Regulatory FactorsMiceMice, Inbred C57BLMice, TransgenicProtein BindingAutoantigensImmunoglobulinsInterferon Regulatory Factor-4Interferon Regulatory Factors

Identifiers

PMID18285461
PMCPMC2293099
OpenAlexW2002429904

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.