Evidence map›Paper›PMID 19494264›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2009

Modulation of p38 MAPK activity in regulatory T cells after tolerance with anti-DNA Ig peptide in (NZB x NZW)F1 lupus mice.

Elaine V Lourenço, Claudio Procaccini, Francesca Ferrera, Noriko Iikuni, Ram P Singh, Gilberto Filaci, Giuseppe Matarese, Fu-Dong Shi, Ernest Brahn, Bevra H Hahn and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

6 citing papers in PubMed, 16 citations in OpenAlex.

  1. Syk inhibitor attenuates lupus in FcγRIIbCell death discovery · 2025
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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

11 authors at 4 institutions in 2 countries.

Elaine V LourençoDivision of Rheumatology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA 90095, USA.
Claudio Procaccini
Francesca Ferrera
Noriko Iikuni
Ram P Singh
Gilberto Filaci
Giuseppe Matarese
Fu-Dong Shi
Ernest Brahn
Bevra H Hahn
Antonio La Cava
University of California, Los Angeles · USAlleanza Contro il Cancro · ITMultiMedica · ITSt. Joseph's Hospital and Medical Center · US

Funding

MECHANISMS OF IMMUNE TOLERANCE INDUCED IN MURINE LUPUSR37AI046776 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HAHN, BEVRA H · 2000 to 2009
$3.9M
Role of Leptin in Systemic Lupus ErythematosusR01AR053239 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LA CAVA, ANTONIO · 2006 to 2010
$1.6M
Molecular Basis of Suppression of SLE by CD8+ Ti CellsR21AI065645 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SINGH, RAM PYARE · 2007 to 2008
$229k
Delineating the Role of Selected Genes in Lupus Induced by CD8+Ti and CD4+CD25 TR03AR054034 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SINGH, RAM PYARE · 2007 to 2009
$228k
IN SITU STUDIES OF COLLAGEN ARTHRITIS AND ANGIOGENESISR01AR042200 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BRAHN, ERNEST · 1994 to 1996
–
IN SITU STUDIES OF COLLAGEN ARTHRITIS AND ANGIOGENESISR55AR042200 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BRAHN, ERNEST · 1993 to 1993
–
European Research Council 202579NIAID NIH HHS AI065645NIAID NIH HHS AI46776NIAID NIH HHS R21 AI065645NIAID NIH HHS R37 AI046776NIAMS NIH HHS AR054034NIAMS NIH HHS AR42200NIAMS NIH HHS AR53239NIAMS NIH HHS R01 AR053239NIAMS NIH HHS R03 AR054034Telethon GJT08004
6 · The paper itself

Abstract

Treatment of (NZB x NZW)F(1) (NZB/W) lupus-prone mice with the anti-DNA Ig-based peptide pConsensus prolongs the survival of treated animals and effectively delays the appearance of autoantibodies and glomerulonephritis. We have previously shown that part of these protective effects associated with the induction of CD4(+)CD25(+)Foxp3(+) regulatory T cells (Tregs) that suppressed autoantibody responses. Because the effects of pConsensus appeared secondary to qualitative rather than quantitative changes in Tregs, we investigated the molecular events induced by tolerance in Tregs and found that signaling pathways including ZAP70, p27, STAT1, STAT3, STAT6, SAPK, ERK, and JNK were not significantly affected. However, peptide tolerization affected in Tregs the activity of the MAPK p38, whose phosphorylation was reduced by tolerance. The pharmacologic inhibition of p38 with the pyridinyl imidazole inhibitor SB203580 in naive NZB/W mice reproduced in vivo the effects of peptide-induced tolerance and protected mice from lupus-like disease. Transfer experiments confirmed the role of p38 in Tregs on disease activity in the NZB/W mice. These data indicate that the modulation of p38 activity in lupus Tregs can significantly influence the disease activity.

Indexed as

AnimalsCD4 Lymphocyte CountDNADown-RegulationEnzyme ActivationFemaleImmune ToleranceImmunoglobulinsLupus Erythematosus, SystemicMicep38 Mitogen-Activated Protein KinasesPeptidesSurvival RateT-Lymphocytes, RegulatoryDNAImmunoglobulinsp38 Mitogen-Activated Protein KinasesPeptides

Identifiers

PMID19494264
PMCPMC2758643
OpenAlexW1493150347

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.