Evidence map›Paper›PMID 28076390›Full record

ArticlePloS one2017

IL-37 Confers Protection against Mycobacterial Infection Involving Suppressing Inflammation and Modulating T Cell Activation.

Haipeng Liu, Ruijuan Zheng, Peng Wang, Hua Yang, Xin He, Qun Ji, Wenjuan Bai, Hao Chen, Jianxia Chen, Wenxia Peng and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Review
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  7. Article
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  10. Article
  11. Article
  12. Interleukin-18 in Health and Disease.International journal of molecular sciences · 2019
    Review
  13. Article
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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

13 authors at 2 institutions in 1 country.

Haipeng LiuShanghai TB Key Laboratory, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China.
Ruijuan ZhengShanghai TB Key Laboratory, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China.
Peng WangDepartment of TB, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China.
Hua YangShanghai TB Key Laboratory, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China.
Xin HeClinical Translational Research Center, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China.
Qun JiClinical Translational Research Center, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China.
Wenjuan BaiShanghai TB Key Laboratory, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China.
Hao ChenDepartment of Microbiology and Immunology, Tongji University School of Medicine, Shanghai, China.
Jianxia ChenShanghai TB Key Laboratory, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China.
Wenxia PengClinical Translational Research Center, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China.
Siyu LiuShanghai TB Key Laboratory, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China.
Zhonghua LiuShanghai TB Key Laboratory, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China.
Baoxue GeShanghai TB Key Laboratory, Shanghai Pulmonary Hospital, Tongji University, Shanghai, China.
Tongji University · CNShanghai Pulmonary Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin-37 (IL-37), a novel member of the IL-1 family, plays fundamental immunosuppressive roles by broadly reducing both innate inflammation and acquired immunity, but whether it is involved in the pathogenesis of tuberculosis (TB) has not been clearly elucidated. In this study, single nucleotide polymorphism (SNP) analysis demonstrated an association of the genetic variant rs3811047 of IL-37 with TB susceptibility. In line with previous report, a significant elevated IL-37 abundance in the sera and increased expression of IL-37 protein in the peripheral blood mononuclear cells (PBMC) were observed in TB patients in comparison to healthy controls. Moreover, release of IL-37 were detected in either macrophages infected with Mycobacterium tuberculosis (Mtb) or the lung of BCG-infected mice, concurrent with reduced production of proinflammatory cytokines including IL-6 and TNF-α. Furthermore, in contrast to wild-type mice, BCG-infected IL-37-Tg mice manifested with reduced mycobacterial burden and tissue damage in the lung, accompanied by higher frequency of Th1 cell and less frequencies of regulatory T cells and Th17 cells in the spleen. Taken together, our findings demonstrated that IL-37 conferred resistance to Mtb infection possibly involving suppressing detrimental inflammation and modulating T cell responses. These findings implicated that IL-37 may be employed as a new molecular target for the therapy and diagnosis of TB.

Indexed as

AnimalsCase-Control StudiesCells, CulturedCytoprotectionFemaleGene FrequencyGenetic Predisposition to DiseaseHumansInflammationInterleukin-1Lymphocyte ActivationMiceMice, Inbred C57BLMice, TransgenicMycobacterium bovisMycobacterium InfectionsIL37 protein, humanInterleukin-1

Identifiers

PMID28076390
PMCPMC5226736
OpenAlexW2577312673

What OpenQuestion holds

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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.