Evidence map›Paper›PMID 16735466›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

A peptide based on the complementarity-determining region 1 of an autoantibody ameliorates lupus by up-regulating CD4+CD25+ cells and TGF-beta.

Amir Sharabi, Heidy Zinger, Maya Zborowsky, Zev M Sthoeger, Edna Mozes

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.5field-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

36 citing papers in PubMed, 87 citations in OpenAlex.

  1. Review
  2. Review
  3. Peptide-based immunotherapy in lupus: Where are we now?Rheumatology and immunology research · 2023
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Getting Under the Skin: Targeting Cutaneous Autoimmune Disease.The Yale journal of biology and medicine · 2020
    Review
  9. Peptide-Based Vaccination Therapy for Rheumatic Diseases.Journal of immunology research · 2020
    Review
  10. Regulatory T cells in the treatment of disease.Nature reviews. Drug discovery · 2018
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
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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

5 authors at 2 institutions in 1 country.

Amir SharabiDepartment of Immunology, Weizmann Institute of Science, Rehovot 76100, Israel.
Heidy Zinger
Maya Zborowsky
Zev M Sthoeger
Edna Mozes
Weizmann Institute of Science · ILKaplan Medical Center · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus is an autoimmune disease characterized by autoantibodies and systemic clinical manifestations. A peptide, designated hCDR1, based on the complementarity-determining region (CDR) 1 of an autoantibody, ameliorated the serological and clinical manifestations of lupus in both spontaneous and induced murine models of lupus. The objectives of the present study were to determine the mechanism(s) underlying the beneficial effects induced by hCDR1. Adoptive transfer of hCDR1-treated cells to systemic lupus erythematosus-afflicted (NZBxNZW)F1 female mice down-regulated all disease manifestations. hCDR1 treatment up-regulated (by 30-40%) CD4+CD25+ cells in association with CD45RBlow, cytotoxic T lymphocyte antigen 4, and Foxp3 expression. Depletion of the CD25+ cells diminished significantly the therapeutic effects of hCDR1, whereas administration of the enriched CD4+CD25+ cell population was beneficial to the diseased mice. Amelioration of disease manifestations was associated with down-regulation of the pathogenic cytokines (e.g., IFN-gamma and IL-10) and up-regulation of the immunosuppressive cytokine TGF-beta, which substantially contributed to the suppressed autoreactivity. TGF-beta was secreted by CD4+ cells that were affected by hCDR1-induced immunoregulatory cells. The hCDR1-induced CD4+CD25+ cells suppressed autoreactive CD4+ cells, resulting in reduced rates of activation-induced apoptosis. Thus, hCDR1 ameliorates lupus through the induction of CD4+CD25+ cells that suppress activation of the autoreactive cells and trigger the up-regulation of TGF-beta.

Indexed as

AnimalsAutoantibodiesCD4-Positive T-LymphocytesCell DeathComplementarity Determining RegionsFemaleHumansImmunotherapy, AdoptiveLupus VulgarisLymphocyte ActivationMicePeptidesReceptors, Interleukin-2SpleenTransforming Growth Factor betaUp-RegulationAutoantibodiesComplementarity Determining RegionsPeptidesReceptors, Interleukin-2Transforming Growth Factor beta

Identifiers

PMID16735466
PMCPMC1482660
OpenAlexW2074751624

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.