Evidence map›Paper›PMID 33710283›Full record

ArticleThe Journal of experimental medicine2021

AIM2 controls microglial inflammation to prevent experimental autoimmune encephalomyelitis.

Chunmei Ma, Sheng Li, Yingchao Hu, Yan Ma, Yuqing Wu, Chunyan Wu, Xue Liu, Bingwei Wang, Gang Hu, Jiawei Zhou and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
6.5field-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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

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  11. Deletion of the X-chromosomal geneScience translational medicine · 2025
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1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Chunmei Ma *Department of Immunology, Key Laboratory of Immunological Environment and Disease, State Key Laboratory of Reproductive Medicine, Center for Global Health, Nanjing Medical University, Nanjing, China.
Sheng Li *Department of Immunology, Key Laboratory of Immunological Environment and Disease, State Key Laboratory of Reproductive Medicine, Center for Global Health, Nanjing Medical University, Nanjing, China.
Yingchao HuDepartment of Immunology, Key Laboratory of Immunological Environment and Disease, State Key Laboratory of Reproductive Medicine, Center for Global Health, Nanjing Medical University, Nanjing, China.
Yan MaDepartment of Pharmacology, Nanjing University of Chinese Medicine, Nanjing, China.
Yuqing WuDepartment of Immunology, Key Laboratory of Immunological Environment and Disease, State Key Laboratory of Reproductive Medicine, Center for Global Health, Nanjing Medical University, Nanjing, China.
Chunyan WuDepartment of Immunology, Key Laboratory of Immunological Environment and Disease, State Key Laboratory of Reproductive Medicine, Center for Global Health, Nanjing Medical University, Nanjing, China.
Xue LiuDepartment of Immunology, Key Laboratory of Immunological Environment and Disease, State Key Laboratory of Reproductive Medicine, Center for Global Health, Nanjing Medical University, Nanjing, China.
Bingwei WangDepartment of Pharmacology, Nanjing University of Chinese Medicine, Nanjing, China.
Gang HuDepartment of Pharmacology, Nanjing University of Chinese Medicine, Nanjing, China.
Jiawei ZhouInstitute of Neuroscience, State Key Laboratory of Neuroscience, Center for Excellence in Brain Science and Intelligence Technology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Shuo YangDepartment of Immunology, Key Laboratory of Immunological Environment and Disease, State Key Laboratory of Reproductive Medicine, Center for Global Health, Nanjing Medical University, Nanjing, China.
State Key Laboratory of Reproductive MedicineNanjing University of Chinese Medicine · CNChinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of the PYHIN family member absent in melanoma 2 (AIM2), another important inflammasome sensor, in EAE remains unclear. In this study, we found that AIM2 negatively regulates the pathogenesis of EAE independent of inflammasome activation. AIM2 deficiency enhanced microglia activation and infiltration of peripheral immune cells into the CNS, thereby promoting neuroinflammation and demyelination during EAE. Mechanistically, AIM2 negatively regulates the DNA-PK-AKT3 in microglia to control neuroinflammation synergistically induced by cGAS and DNA-PK. Administration of a DNA-PK inhibitor reduced the severity of the EAE. Collectively, these findings identify a new role for AIM2 in controlling the onset of EAE. Furthermore, delineation of the underlying inflammasome-independent mechanism highlights cGAS and DNA-PK signaling as potential targets for the treatment of heterogeneous MS.

Indexed as

AnimalsAnimals, NewbornCells, CulturedCentral Nervous SystemDNA-Activated Protein KinaseDNA-Binding ProteinsEncephalomyelitis, Autoimmune, ExperimentalFemaleGene ExpressionInflammasomesInflammationMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMicrogliaAim2 protein, mouseAkt3 protein, mouseDNA-Activated Protein KinaseDNA-Binding ProteinsInflammasomesPrkdc protein, mouseProto-Oncogene Proteins c-akt

Identifiers

PMID33710283
PMCPMC7961553
OpenAlexW3135533983

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.