Evidence map›Paper›PMID 9927509›Full record

ArticleThe Journal of experimental medicine1999

Severe attenuation of the B cell immune response in Msh2-deficient mice.

K A Vora, K M Tumas-Brundage, V M Lentz, A Cranston, R Fishel, T Manser

Abstract read
In one paragraph

Article in The Journal of experimental medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
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

28 citing papers in PubMed.

  1. Article
  2. Article
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  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Somatic immunoglobulin hypermutation.Current opinion in immunology · 2002
    Review
  18. Article
  19. Switch junction sequences in PMS2-deficient mice reveal a microhomology-mediated mechanism of Ig class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2001
    Article
  20. 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

6 authors.

K A VoraDepartment of Microbiology and Immunology and The Kimmel Cancer Institute, Jefferson Medical College, Philadelphia, Pennsylvania 19107, USA.
K M Tumas-Brundage
V M Lentz
A Cranston
R Fishel
T Manser

Funding

The Human Mismatch Repair Proteins and CarcinogenesisR01CA067007 · NCI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI Richard Fishel · 1995 to 2026
$9.6M
TRAINING PROGRAMS IN MOLECULAR GENETICS OF CANCERT32CA009678 · NCI · THOMAS JEFFERSON UNIVERSITY · PI BUCHBERG, ARTHUR M. · 1992 to 2008
$2.3M
RECOMBINATION/REPAIR COMPLEX IN HUMAN CELLSR01CA056542 · NCI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI FISHEL, RICHARD · 1993 to 2005
$2.3M
TRAINING PROGRAM IN DEVELOPMENTAL IMMUNOLOGYT32AI007492 · NIAID · THOMAS JEFFERSON UNIVERSITY · PI MANSER, TIMOTHY L · 1996 to 2005
$1.3M
EXPRESSION OF ANTIBODY DIVERSITY DURING IMMUNE RESPONSESR01AI023739 · NIAID · THOMAS JEFFERSON UNIVERSITY · PI MANSER, TIMOTHY L · 1986 to 2001
$481k
NCI NIH HHS CA56542NCI NIH HHS CA67007NCI NIH HHS R01 CA056542NCI NIH HHS R01 CA067007NCI NIH HHS T32 CA009678NIAID NIH HHS AI23739NIAID NIH HHS T32 AI007492
6 · The paper itself

Abstract

Recently, results obtained from mice with targeted inactivations of postreplication DNA mismatch repair (MMR) genes have been interpreted to demonstrate a direct role for MMR in antibody variable (V) gene hypermutation. Here we show that mice that do not express the MMR factor Msh2 have wide-ranging defects in antigen-driven B cell responses. These include lack of progression of the germinal center (GC) reaction associated with increased intra-GC apoptosis, severely diminished antigen-specific immunoglobulin G responses, and near absence of anamnestic responses. Mice heterozygous for the Msh2 deficiency display an "intermediate" phenotype in these regards, suggesting that normal levels of Msh2 expression are critical for the B cell response. Interpretation of the impact of an MMR deficiency on the mechanism of V gene somatic hypermutation could be easily confounded by these perturbations.

Indexed as

DNA-Binding ProteinsDNA RepairLymphocyte ActivationAnimalsAntibodiesApoptosisB-LymphocytesBone Marrow CellsGerminal CenterHeterozygoteHomozygoteImmune SystemImmunoglobulin Class SwitchingImmunoglobulin IsotypesMiceMice, Mutant StrainsAntibodiesDNA-Binding ProteinsImmunoglobulin IsotypesMsh2 protein, mouseMutS Homolog 2 ProteinProto-Oncogene Proteins

Identifiers

PMID9927509
PMCPMC2192912

What OpenQuestion holds

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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.