Evidence map›Paper›PMID 21287397›Full record

ArticleJournal of clinical immunology2011

The histone peptide H4 71-94 alone is more effective than a cocktail of peptide epitopes in controlling lupus: immunoregulatory mechanisms.

Hee-Kap Kang, Ming-Yi Chiang, Michael Liu, Diane Ecklund, Syamal K Datta

Abstract read
In one paragraph

Article in Journal of clinical immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Vaccines for immune tolerance against autoimmune disease.Advanced drug delivery reviews · 2023
    Review
  3. Review
  4. Article
  5. CD8Rheumatology and immunology research · 2021
    Review
  6. Review
  7. Review
  8. Peptide-Based Vaccination Therapy for Rheumatic Diseases.Journal of immunology research · 2020
    Review
  9. Article
  10. Normalization of CD4+ T cell metabolism reverses lupus.Science translational medicine · 2015
    Article
  11. 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

5 authors at 1 institution in 1 country.

Hee-Kap KangDivision of Rheumatology, Department of Medicine, Northwestern University Feinberg School of Medicine, 240 East Huron St. McGaw # M300, Chicago, IL 60611, USA.
Ming-Yi Chiang
Michael Liu
Diane Ecklund
Syamal K Datta
Northwestern University · US

Funding

MULTIDISCIPLINARY CLINICAL AND TRANSLATIONAL SCIENCE (MCTS) PROGRAM (UL1)UL1RR025741 · NCRR · NORTHWESTERN UNIVERSITY AT CHICAGO · PI GREENLAND, PHILIP · 2008 to 2011
$24.7M
Unconventional APC Inducing Autoimmune Th17 Cell Expansion in LupusR01AI041985 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI DATTA, SYAMAL K · 1997 to 2014
$4.3M
MECHANISM OF AUTOIMMUNE RESPONSE IN HUMAN LUPUSR37AR039157 · NIAMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI DATTA, SYAMAL K · 2000 to 2009
$2.8M
NCRR NIH HHS UL1 RR025741NIAID NIH HHS R01 AI041985NIAID NIH HHS R01-AI41985NIAMS NIH HHS R37 AR039157NIAMS NIH HHS R37-AR39157
6 · The paper itself

Abstract

Tolerance therapy with nucleosomal histone peptides H4(71-94), H4(16-39), or H1'(22-42) controls disease in lupus-prone SNF1 mice. It would be clinically important to determine whether a cocktail of the above epitopes would be superior. Herein, we found that compared with cocktail peptides, H4(71-94) monotherapy more effectively delayed nephritis onset, prolonged lifespan, diminished immunoglobulin G autoantibody levels, reduced autoantigen-specific Th1 and Th17 responses and frequency of T(FH) cells in spleen and the helper ability of autoimmune T cells to B cells, by inducing potent CD8 Treg cells. H4(71-94) therapy was superior in "tolerance spreading," suppressing responses to other autoepitopes, nucleosomes, and ribonucleoprotein. We also developed an in vitro assay for therapeutic peptides (potentially in humans), which showed that H4(71-94), without exogenous transforming growth factor (TGF)-β, was efficient in inducing stable CD4(+)CD25(+)Foxp3(+) T cells by decreasing interleukin 6 and increasing TGF-β production by dendritic cells that induced ALK5-dependent Smad-3 phosphorylation (TGF-β signal) in target autoimmune CD4(+) T cells.

Indexed as

ImmunoassayAnimalsAutoantibodiesAutoantigensAutoimmunityB-LymphocytesCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCytokinesDendritic CellsDisease Models, AnimalDrug CombinationsEpitopesFemaleFlow CytometryHistonesAutoantibodiesAutoantigensCytokinesDrug CombinationsEpitopesHistonesImmunologic FactorsNucleosomesPeptides

Identifiers

PMID21287397
PMCPMC3125430
OpenAlexW1972759583

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.