Evidence map›Paper›PMID 20194724›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

Triptolide inhibits IL-12/IL-23 expression in APCs via CCAAT/enhancer-binding protein alpha.

Yan Zhang, Xiaojing Ma

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
11.6field-weighted citation impact, top 2% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. A comprehensive review ofFrontiers in pharmacology · 2023
    Review
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  7. Mechanism for the therapeutic effect ofZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022
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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

2 authors at 1 institution in 1 country.

Yan ZhangDepartment of Microbiology and Immunology, Weill Medical College, eill Graduate School of Medical Sciences, Cornell University, New York, NY 10065, USA.
Xiaojing Ma
Cornell University · US

Funding

Regulation of IL-12 Expression and Activity by OncogenesR01CA100223 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI MA, XIAOJING · 2004 to 2008
$1.5M
Mechanism of Modulation of Interleukin-12 Production by TriptolideR21AT004349 · NCCIH · WEILL MEDICAL COLL OF CORNELL UNIV · PI MA, XIAOJING · 2007 to 2008
$431k
NCCIH NIH HHS R21 AT004349NCI NIH HHS R01 CA100223
6 · The paper itself

Abstract

Triptolide is a biologically active component purified from Chinese herbal plant Tripterygium wilfordii Hook F. It is widely used in East Asia for treatment of systemic lupus erythematosus, rheumatoid arthritis, nephritis, Bechect's disease, psoriasis, atopic dermatitis, and asthma. However, its immunological mechanisms are poorly understood. IL-12 and IL-23 are closely related heterodimeric cytokines that share the common subunit p40. They are produced by APCs and are key factors in the generation and effector functions of Th1 and Th17 cells, respectively. They have been strongly implicated in the pathogenesis of several autoimmune disorders. In this study, we investigated the molecular mechanism whereby triptolide inhibits the expression of the p40 gene in APCs. We demonstrate that triptolide does so at the transcriptional level in part through targeting CCAAT/enhancer-binding protein-alpha (C/EBPalpha), which directly interacts with the p40 promoter and inhibits its transcription in inflammatory macrophages. Triptolide can activate the transcription of C/EBPalpha, and phosphorylation of Ser21 and Thr222/226 critical for C/EBPalpha inhibition of p40. Further, activation of C/EBPalpha by triptolide is dependent on upstream kinases ERK1/2 and Akt-GSK3beta. This study provides mechanistic insights into the immunomodulatory capacity of triptolide and has strong implications for its therapeutic applications in autoimmune diseases.

Indexed as

AnimalsAntigen-Presenting CellsCCAAT-Enhancer-Binding Protein-alphaDiterpenesElectrophoretic Mobility Shift AssayEnzyme-Linked Immunosorbent AssayEpoxy CompoundsGene ExpressionHumansImmunodominant EpitopesImmunosuppressive AgentsInterleukin-12Interleukin-23MiceMice, KnockoutOligonucleotide Array Sequence AnalysisCCAAT-Enhancer-Binding Protein-alphaDiterpenesEpoxy CompoundsImmunodominant EpitopesImmunosuppressive AgentsInterleukin-12Interleukin-23P40, iodinated C-terminal peptide, humanPeptide FragmentsPhenanthrenestriptolide

Identifiers

PMID20194724
PMCPMC2965075
OpenAlexW2131551079

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.