Evidence map›Paper›PMID 15738053›Full record

ArticleThe Journal of experimental medicine2005

An immunoglobulin C kappa-reactive single chain antibody fusion protein induces tolerance through receptor editing in a normal polyclonal immune system.

Djemel Ait-Azzouzene, Laurent Verkoczy, Jorieke Peters, Amanda Gavin, Patrick Skog, José Luis Vela, David Nemazee

Abstract read
In one paragraph

Article in The Journal of experimental medicine, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing 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

44 citing papers in PubMed.

  1. Article
  2. Distributed Clonal Deletion Prevents Autoimmune Disease Progression.bioRxiv : the preprint server for biology · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Heavy-chain receptor editing unbound.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  18. Article
  19. VH replacement in primary immunoglobulin repertoire diversification.Proceedings of the National Academy of Sciences of the United States of America · 2015
    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

7 authors.

Djemel Ait-AzzouzeneDepartment of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA.
Laurent Verkoczy
Jorieke Peters
Amanda Gavin
Patrick Skog
José Luis Vela
David Nemazee

Funding

BLOOD SYSTEMS IN COAGULATION AND VESSEL DISEASET32HL007195 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI RUF, WOLFRAM · 1985 to 2011
$5.1M
Immune Tolerance in Non-Clonal Immune SystemsR01AI059714 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI NEMAZEE, DAVID · 2004 to 2013
$3.9M
RECEPTOR EDITING IN B-CELLSR01AI033608 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI NEMAZEE, DAVID · 1993 to 2010
$3.7M
Immune Tolerance in Non-clonal Immune SystemsR21AI049940 · NIAID · SCRIPPS RESEARCH INSTITUTE · PI NEMAZEE, DAVID · 2001 to 2003
$785k
MINORITY PREDOCTORAL FELLOWSHIP PROGRAMF31AI052484 · NIAID · SCRIPPS RESEARCH INSTITUTE · PI VELA, JOSE L · 2002 to 2004
$80k
NHLBI NIH HHS T32 HL007195NHLBI NIH HHS T32 HL07195NIAID NIH HHS F31 AI052484NIAID NIH HHS F31 AI52484NIAID NIH HHS R01 AI033608NIAID NIH HHS R01 AI059714NIAID NIH HHS R01AI59714NIAID NIH HHS R21AI49940
6 · The paper itself

Abstract

Understanding immune tolerance mechanisms is a major goal of immunology research, but mechanistic studies have generally required the use of mouse models carrying untargeted or targeted antigen receptor transgenes, which distort lymphocyte development and therefore preclude analysis of a truly normal immune system. Here we demonstrate an advance in in vivo analysis of immune tolerance that overcomes these shortcomings. We show that custom superantigens generated by single chain antibody technology permit the study of tolerance in a normal, polyclonal immune system. In the present study we generated a membrane-tethered anti-Igkappa-reactive single chain antibody chimeric gene and expressed it as a transgene in mice. B cell tolerance was directly characterized in the transgenic mice and in radiation bone marrow chimeras in which ligand-bearing mice served as recipients of nontransgenic cells. We find that the ubiquitously expressed, Igkappa-reactive ligand induces efficient B cell tolerance primarily or exclusively by receptor editing. We also demonstrate the unique advantages of our model in the genetic and cellular analysis of immune tolerance.

Indexed as

AnimalsAutoantigensB-LymphocytesBone Marrow CellsBone Marrow TransplantationCell Line, TumorGenes, RAG-1Immune SystemImmune ToleranceImmunoglobulin kappa-ChainsImmunoglobulin lambda-ChainsMiceMice, KnockoutMice, TransgenicMutationProto-Oncogene Proteins c-bcl-2AutoantigensImmunoglobulin kappa-ChainsImmunoglobulin lambda-ChainsProto-Oncogene Proteins c-bcl-2Recombinant Fusion Proteins

Identifiers

PMID15738053
PMCPMC2212821

What OpenQuestion holds

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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.