Evidence map›Paper›PMID 7533792›Full record

ArticleThe Journal of clinical investigation1995

Somatic mutation of human immunoglobulin V genes in the X-linked HyperIgM syndrome.

Y W Chu, E Marin, R Fuleihan, N Ramesh, F S Rosen, R S Geha, R A Insel

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 7% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Hyper IgM Syndrome: a Report from the USIDNET Registry.Journal of clinical immunology · 2016
    Article
  5. Article
  6. Article
  7. Article
  8. CD40-CD40L independent Ig gene hypermutation suggests a second B cell diversification pathway in humans.Proceedings of the National Academy of Sciences of the United States of America · 2001
    Article
  9. Article
  10. Article
  11. Article
  12. The hyper-IgM (HIM) syndrome.Springer seminars in immunopathology · 1998
    Review
  13. Article
  14. Memory B lymphocytes migrate to bone marrow in humans.Proceedings of the National Academy of Sciences of the United States of America · 1997
    Article
  15. Article
  16. 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

7 authors at 2 institutions in 1 country.

Y W ChuDepartment of Pediatrics, Microbiology, and Immunology, University of Rochester School of Medicine and Dentistry, New York 14642.
E Marin
R Fuleihan
N Ramesh
F S Rosen
R S Geha
R A Insel
Harvard University · USUniversity of Rochester · US

Funding

TRANSGENIC MODELS OF T CELL RECEPTOR IMMUNODEFICIENCIESP01AI035714 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TERHORST, CORNELIS P · 1994 to 2007
$9.3M
MECHANISMS OF IGE SYNTHESIS BY HUMAN B CELLSR01AI031136 · NIAID · CHILDREN'S HOSPITAL BOSTON · PI GEHA, RAIF SALIM · 1992 to 2007
$1.9M
DEVELOPMENT OF ANTIBODY REPERTOIRES TO POLYSACCHARIDESR01AI037123 · NIAID · UNIVERSITY OF ROCHESTER · PI INSEL, RICHARD A. · 1994 to 2000
$242k
NIAID NIH HHS AI31136NIAID NIH HHS AI35714NIAID NIH HHS AI37123
6 · The paper itself

Abstract

Somatic mutation of Ig variable regions occurs prominently in germinal centers, but it has been debated whether the mutation process initiates in germinal centers or is activated before germinal center entry of B cells. We have analyzed for the presence of somatic mutation in Ig gene rearrangements of the nonpolymorphic human VH6 gene in the X-linked HyperIgM syndrome, which is associated with defective CD40 ligand expression and absence of germinal centers and generation of memory B lymphocytes. IgM and rare IgG VH6 productive rearrangements were isolated from PBL of patients with X-linked HyperIgM syndrome. Although the majority of both the IgM and IgG VH6 rearrangements had a germline VH6 sequence, 7 of 102 VH6 IgM and 1 of 6 IgG rearrangements had a mutated VH6 gene. The mutation frequency (mutations/bp) was 1.4% with a range of 2-9 mutations per clone, a mutation frequency lower, however, than that observed in IgM (3.2%) and IgG (5.4%) VH6 rearrangements of normal individuals. These results suggest that somatic mutation may be initiated in a CD40 ligand-independent pathway before entry of B cells into germinal centers, but fails to achieve the high mutation frequency observed in the presence of germinal centers.

Indexed as

Amino Acid SequenceAntigens, CDAntigens, Differentiation, B-LymphocyteAutoimmune DiseasesBase SequenceCD40 AntigensGene RearrangementGenes, ImmunoglobulinGenetic LinkageHumansImmunoglobulin MImmunoglobulin Variable RegionImmunologic Deficiency SyndromesLymphocytesMolecular Sequence DataMutationAntigens, CDAntigens, Differentiation, B-LymphocyteCD40 AntigensImmunoglobulin MImmunoglobulin Variable RegionRNA, Messenger

Identifiers

PMID7533792
PMCPMC441480
OpenAlexW2165754415

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.