Evidence map›Paper›PMID 25329476›Full record

ArticlePLoS pathogens2014

Allele-specific induction of IL-1β expression by C/EBPβ and PU.1 contributes to increased tuberculosis susceptibility.

Guoliang Zhang, Boping Zhou, Shaoyuan Li, Jun Yue, Hui Yang, Yuxin Wen, Senlin Zhan, Wenfei Wang, Mingfeng Liao, Mingxia Zhang and 4 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

82 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.

  1. Pooled it
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  17. The PE/PPE family proteins ofFrontiers in immunology · 2025
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22 more citing papers are in PubMed but not listed here.

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

14 authors at 5 institutions in 2 countries.

Guoliang ZhangGuangdong Key Lab of Emerging Infectious Diseases, Guangdong Medical College, Shenzhen, China; Shenzhen Key Lab of Infection and Immunity, Shenzhen Third People's Hospital, Guangdong Medical College, Shenzhen, China.
Boping ZhouGuangdong Key Lab of Emerging Infectious Diseases, Guangdong Medical College, Shenzhen, China.
Shaoyuan LiDepartment of Microbiology, Key Laboratory for Tropical Diseases Control of the Ministry of Education, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Jun YueDepartment of Clinical Laboratory, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China.
Hui YangShenzhen Key Lab of Infection and Immunity, Shenzhen Third People's Hospital, Guangdong Medical College, Shenzhen, China.
Yuxin WenDepartment of Chest Surgery, Shenzhen People's Hospital, Jinan University, Shenzhen, China.
Senlin ZhanGuangdong Key Lab of Emerging Infectious Diseases, Guangdong Medical College, Shenzhen, China; Shenzhen Key Lab of Infection and Immunity, Shenzhen Third People's Hospital, Guangdong Medical College, Shenzhen, China.
Wenfei WangGuangdong Key Lab of Emerging Infectious Diseases, Guangdong Medical College, Shenzhen, China; Shenzhen Key Lab of Infection and Immunity, Shenzhen Third People's Hospital, Guangdong Medical College, Shenzhen, China.
Mingfeng LiaoGuangdong Key Lab of Emerging Infectious Diseases, Guangdong Medical College, Shenzhen, China; Shenzhen Key Lab of Infection and Immunity, Shenzhen Third People's Hospital, Guangdong Medical College, Shenzhen, China.
Mingxia ZhangGuangdong Key Lab of Emerging Infectious Diseases, Guangdong Medical College, Shenzhen, China; Shenzhen Key Lab of Infection and Immunity, Shenzhen Third People's Hospital, Guangdong Medical College, Shenzhen, China.
Gucheng ZengDepartment of Microbiology, Key Laboratory for Tropical Diseases Control of the Ministry of Education, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Carl G FengDepartment of Infectious Diseases and Immunology, Sydney Medical School, The University of Sydney, Sydney, Australia.
Christopher M SassettiDepartment of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, Massachusetts, United States of America; Howard Hughes Medical Institute, Chevy Chase, Maryland, United States of America.
Xinchun ChenGuangdong Key Lab of Emerging Infectious Diseases, Guangdong Medical College, Shenzhen, China; Shenzhen Key Lab of Infection and Immunity, Shenzhen Third People's Hospital, Guangdong Medical College, Shenzhen, China.
Guangdong Medical College · CNSun Yat-sen University · CNJinan University · CNTongji University · CNUniversity of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mycobacterium tuberculosis infection is associated with a spectrum of clinical outcomes, from long-term latent infection to different manifestations of progressive disease. Pro-inflammatory pathways, such as those controlled by IL-1β, have the contrasting potential both to prevent disease by restricting bacterial replication, and to promote disease by inflicting tissue damage. Thus, the ultimate contribution of individual inflammatory pathways to the outcome of M. tuberculosis infection remains ambiguous. In this study, we identified a naturally-occurring polymorphism in the human IL1B promoter region, which alters the association of the C/EBPβ and PU.1 transcription factors and controls Mtb-induced IL-1β production. The high-IL-1β expressing genotype was associated with the development of active tuberculosis, the severity of pulmonary disease and poor treatment outcome in TB patients. Higher IL-1β expression did not suppress the activity of IFN-γ-producing T cells, but instead correlated with neutrophil accumulation in the lung. These observations support a specific role for IL-1β and granulocytic inflammation as a driver of TB disease progression in humans, and suggest novel strategies for the prevention and treatment of tuberculosis.

Indexed as

AllelesCCAAT-Enhancer-Binding Protein-betaCell LineDisease SusceptibilityHumansInterferon-gammaInterleukin-1betaLungProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Trans-ActivatorsTuberculosisCCAAT-Enhancer-Binding Protein-betaInterferon-gammaInterleukin-1betaProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Trans-Activators

Identifiers

PMID25329476
PMCPMC4199770
OpenAlexW2071876961

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.