Evidence map›Paper›PMID 21482740›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

Transcriptional suppression of IL-27 production by Mycobacterium tuberculosis-activated p38 MAPK via inhibition of AP-1 binding.

Jidong Zhang, Xuesong Qian, Huan Ning, Christopher S Eickhoff, Daniel F Hoft, Jianguo Liu

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

16 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Interleukin-27 Functional Duality BalancesFrontiers in immunology · 2020
    Review
  10. Protein kinase p38α signaling in dendritic cells regulates colon inflammation and tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
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.

Jidong ZhangDivision of Infectious Diseases, Allergy, and Immunology, Department of Internal Medicine, Saint Louis University School of Medicine, St. Louis, MO 63104, USA.
Xuesong Qian
Huan Ning
Christopher S Eickhoff
Daniel F Hoft
Jianguo Liu
Saint Louis University · US

Funding

Role of gammadelta T Cells in Vaccine-Induced ImmunityR01AI048391 · NIAID · SAINT LOUIS UNIVERSITY · PI HOFT, DANIEL F. · 2002 to 2019
$6.1M
NIAID NIH HHS AI048391NIAID NIH HHS R01 AI048391
6 · The paper itself

Abstract

Mycobacterium tuberculosis remains a major global challenge to human health care, and the mechanisms of how M. tuberculosis evades host immune surveillance to favor its survival are still largely unknown. In this study, we found that bacillus Calmette-Guérin (BCG) and viable M. tuberculosis as well as M. tuberculosis lysates could activate IL-27 expression in human and mouse macrophages by induction of p28 subunit transcription. However, in parallel with these effects, BCG and M. tuberculosis lysate stimulation of macrophages induced activation of p38 MAPK signaling molecules MLK3/MKK3/MK2 to prevent maximal IL-27 production. M. tuberculosis lysate-induced p28 transcription was dependent on MyD88 signaling pathway. AP-1/c-Fos was shown to bind directly to the p28 promoter and induce p28 expression after M. tuberculosis lysate stimulation. Overexpression of p38α inhibited the binding of c-Fos to the p28 promoter but had no effect on c-Fos protein expression or phosphorylation in response to M. tuberculosis lysate stimulation. Furthermore, blockade of p38 by SB203580 enhanced M. tuberculosis-induced AP-1 binding to the p28 promoter. Importantly, we show that adding exogenous IL-27 to increase the levels produced by PBMCs stimulated with live mycobacteria enhanced the ability of BCG-expanded T cells to inhibit intracellular mycobacterial growth in human macrophages. Taken together, our data demonstrate that mycobacterial stimulation induces both IL-27 production and p38 MAPK activation. Strategies designed to tip the balance toward positive regulation of p28 induction by mycobacteria could lead to enhanced protective tuberculosis immunity.

Indexed as

Transcription, GeneticAnimalsCell LineChromatin ImmunoprecipitationEnzyme-Linked Immunosorbent AssayFlow CytometryHumansImidazolesInterleukin-17InterleukinsMacrophagesMAP Kinase Signaling SystemMiceMitogen-Activated Protein Kinase 14Mycobacterium bovisMycobacterium tuberculosisIl27 protein, mouseImidazolesInterleukin-17InterleukinsMitogen-Activated Protein Kinase 14Myeloid Differentiation Factor 88p38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-fosPyridinesSB 203580Transcription Factor AP-1

Identifiers

PMID21482740
PMCPMC3150584
OpenAlexW2128672349

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.