Evidence map›Paper›PMID 24211843›Full record

ArticleClinical immunology (Orlando, Fla.)2013

Major pathogenic steps in human lupus can be effectively suppressed by nucleosomal histone peptide epitope-induced regulatory immunity.

Li Zhang, Anne M Bertucci, Rosalind Ramsey-Goldman, Elizabeth Randall Harsha-Strong, Richard K Burt, Syamal K Datta

Open access · greenAbstract read
In one paragraph

Article in Clinical immunology (Orlando, Fla.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Peptide-based immunotherapy in lupus: Where are we now?Rheumatology and immunology research · 2023
    Review
  3. CD8Immunity · 2023
    Article
  4. Article
  5. Review
  6. CD8Rheumatology and immunology research · 2021
    Review
  7. Review
  8. Review
  9. Peptide-Based Vaccination Therapy for Rheumatic Diseases.Journal of immunology research · 2020
    Review
  10. Future prospects for CD8Immunological reviews · 2019
    Review
  11. Review
  12. Tregs in SLE: an Update.Current rheumatology reports · 2018
    Review
  13. Description of CD8Journal of immunology research · 2018
    Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Drugs in early clinical development for Systemic Lupus Erythematosus.Expert opinion on investigational drugs · 2016
    Review
  19. 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 at 1 institution in 1 country.

Li ZhangDivisions of Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Anne M Bertucci
Rosalind Ramsey-Goldman
Elizabeth Randall Harsha-Strong
Richard K Burt
Syamal K Datta
Northwestern University · US

Funding

Multidisciplinary Clinical and Translational Science (MCTS) Program (UL1)UL1TR000150 · NCATS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LLOYD-JONES, DONALD M · 2012 to 2013
$10.1M
Unconventional APC Inducing Autoimmune Th17 Cell Expansion in LupusR01AI041985 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI DATTA, SYAMAL K · 1997 to 2014
$4.3M
SUPERANTIGEN INTERACTIONS WITH MHC CLASS II ANTIGENSP60AR030692 · NIAMS · NORTHWESTERN UNIVERSITY · PI POPE, RICHARD M. · 1986 to 2001
$2.1M
NCATS NIH HHS UL1 TR000150NIAID NIH HHS R01 AI041985NIAID NIH HHS R01AI41985NIAMS NIH HHS P60 AR030692
6 · The paper itself

Abstract

Low-dose tolerance therapy with nucleosomal histone peptide epitopes blocks lupus disease in mouse models, but effect in humans is unknown. Herein, we found that CD4(+)CD25(high)FoxP3(+) or CD4(+)CD45RA(+)FoxP3(low) T-cells, and CD8(+)CD25(+)FoxP3(+) T-cells were all induced durably in PBMCs from inactive lupus patients and healthy subjects by the histone peptide/s themselves, but in active lupus, dexamethasone or hydroxychloroquine unmasked Treg-induction by the peptides. The peptide-induced Treg depended on TGFβ/ALK-5/pSmad 2/3 signaling, and they expressed TGF-β precursor LAP. Lupus patients' sera did not inhibit Treg induction. The peptide epitope-induced T cells markedly suppressed type I IFN related gene expression in lupus PBMC. Finally, the peptide epitopes suppressed pathogenic autoantibody production by PBMC from active lupus patients to baseline levels by additional mechanisms besides Treg induction, and as potently as anti-IL6 antibody. Thus, low-dose histone peptide epitopes block pathogenic autoimmune response in human lupus by multiple mechanisms to restore a stable immunoregulatory state.

Indexed as

AdultAntigens, CDAnti-Inflammatory AgentsAutoantibodiesAutoimmunityCD8-Positive T-LymphocytesEpitopesFemaleForkhead Transcription FactorsGene Expression RegulationHistonesHumansLupus Erythematosus, SystemicLymphocyte ActivationMaleMiddle AgedAntigens, CDAnti-Inflammatory AgentsAutoantibodiesEpitopesForkhead Transcription FactorsFOXP3 protein, humanHistonesNucleosomesPeptidesProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type ISmad2 ProteinSMAD2 protein, humanSmad3 ProteinSMAD3 protein, humanTGFBR1 protein, humanTgfbr1 protein, mouseTransforming Growth Factor beta1,25-dihydroxyvitamin D31,25(OH)(2)D(3)APGApigeninAutoimmunityDEXdexamethasoneHHCQhematopoietic stem cell transplantationhistoneHSCTHumanhydroxychloroquineinduced regulatory T cellsiTregLAPlatency associated peptideODNoligonucleotide.Peptide epitopesRARAPARapamycinretinoic acidSLEsystemic lupus erythematosusSystemic lupus erythematosusT cellsToleranceTrichostatin ATSA

Identifiers

PMID24211843
PMCPMC3849335
OpenAlexW2091101809

What OpenQuestion holds

Textmetadata
LicenceTDM
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.