Evidence map›Paper›PMID 29180626›Full record

ArticleNature communications2017

Mitochondrial dynamics controls anti-tumour innate immunity by regulating CHIP-IRF1 axis stability.

Zhengjun Gao, Yiyuan Li, Fei Wang, Tao Huang, Keqi Fan, Yu Zhang, Jiangyan Zhong, Qian Cao, Tong Chao, Junling Jia and 6 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

80 citing papers in PubMed, 136 citations in OpenAlex.

  1. Review
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20 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

16 authors at 5 institutions in 2 countries.

Zhengjun GaoLife Sciences Institute, Zhejiang University, Hangzhou, 310058, China.
Yiyuan LiLife Sciences Institute, Zhejiang University, Hangzhou, 310058, China.
Fei WangLife Sciences Institute, Zhejiang University, Hangzhou, 310058, China.
Tao HuangLife Sciences Institute, Zhejiang University, Hangzhou, 310058, China.
Keqi FanLife Sciences Institute, Zhejiang University, Hangzhou, 310058, China.
Yu ZhangSir Run Run Shaw Hospital, College of Medicine Zhejiang University, Hangzhou, 310016, China.
Jiangyan ZhongLife Sciences Institute, Zhejiang University, Hangzhou, 310058, China.
Qian CaoSir Run Run Shaw Hospital, College of Medicine Zhejiang University, Hangzhou, 310016, China.
Tong ChaoLife Sciences Institute, Zhejiang University, Hangzhou, 310058, China.
Junling JiaLife Sciences Institute, Zhejiang University, Hangzhou, 310058, China.
Shuo YangDepartment of Immunology, Nanjing Medical University, Nanjing, 211166, Jiangsu Province, China.
Long ZhangLife Sciences Institute, Zhejiang University, Hangzhou, 310058, China.ORCID http://orcid.org/0000-0001-8139-0474
Yichuan XiaoInstitute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences/Shanghai Jiao Tong University School of Medicine, Shanghai, 200031, China.
Ji-Yong ZhouKey Laboratory of Animal Virology of Ministry of Agriculture, Zhejiang University, Hangzhou, 310058, China.
Xin-Hua FengLife Sciences Institute, Zhejiang University, Hangzhou, 310058, China.
Jin JinLife Sciences Institute, Zhejiang University, Hangzhou, 310058, China. jjin4@zju.edu.cn.
Zhejiang University · CNSir Run Run Shaw Hospital · CNMinistry of Agriculture · LVNanjing Medical University · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages, dendritic cells and other innate immune cells are involved in inflammation and host defense against infection. Metabolic shifts in mitochondrial dynamics may be involved in Toll-like receptor agonist-mediated inflammatory responses and immune cell polarization. However, whether the mitochondrial morphology in myeloid immune cells affects anti-tumor immunity is unclear. Here we show that FAM73b, a mitochondrial outer membrane protein, has a pivotal function in Toll-like receptor-regulated mitochondrial morphology switching from fusion to fission. Switching to mitochondrial fission via ablation of Fam73b (also known as Miga2) promotes IL-12 production. In tumor-associated macrophages, this switch results in T-cell activation and enhances anti-tumor immunity. We also show that the mitochondrial morphology affects Parkin expression and its recruitment to mitochondria. Parkin controls the stability of the downstream CHIP-IRF1 axis through proteolysis. Our findings identify mechanisms associated with mitochondrial dynamics that control anti-tumor immune responses and that are potential targets for cancer immunotherapy.

Indexed as

Immunity, InnateAnimalsFemaleHumansInterferon Regulatory Factor-1Interleukin-12Lymphocyte ActivationMacrophagesMaleMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutMitochondriaMitochondrial DynamicsMitochondrial ProteinsInterferon Regulatory Factor-1Interleukin-12Irf1 protein, mouseMembrane ProteinsMitochondrial Proteinsmitoguardin-2 protein, mouseparkin proteinStub1 protein, mouseToll-Like ReceptorsUbiquitin-Protein Ligases

Identifiers

PMID29180626
PMCPMC5703766
OpenAlexW2768841642

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.