Evidence map›Paper›PMID 34718337›Full record

ArticleCell death & disease2021

TNF-α-induced protein 8-like 2 negatively regulates the immune function of dendritic cells by suppressing autophagy via the TAK1/JNK pathway in septic mice.

Shuang-Qing Liu, Chao Ren, Ren-Qi Yao, Yao Wu, Ying-Yi Luan, Ning Dong, Yong-Ming Yao

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

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  14. USP9x promotes CD8Acta biochimica et biophysica Sinica · 2022
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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

7 authors at 1 institution in 1 country.

Shuang-Qing LiuDepartment of Emergency, the Fourth Medical Center of the Chinese PLA General Hospital, 100048, Beijing, People's Republic of China.ORCID 0000-0002-6701-9625
Chao RenTranslational Medicine Research Center, Medical Innovation Research Division and Fourth Medical Center of the Chinese PLA General Hospital, 100048, Beijing, People's Republic of China.
Ren-Qi YaoTranslational Medicine Research Center, Medical Innovation Research Division and Fourth Medical Center of the Chinese PLA General Hospital, 100048, Beijing, People's Republic of China.
Yao WuTranslational Medicine Research Center, Medical Innovation Research Division and Fourth Medical Center of the Chinese PLA General Hospital, 100048, Beijing, People's Republic of China.
Ying-Yi LuanTranslational Medicine Research Center, Medical Innovation Research Division and Fourth Medical Center of the Chinese PLA General Hospital, 100048, Beijing, People's Republic of China.
Ning DongTranslational Medicine Research Center, Medical Innovation Research Division and Fourth Medical Center of the Chinese PLA General Hospital, 100048, Beijing, People's Republic of China.
Yong-Ming YaoTranslational Medicine Research Center, Medical Innovation Research Division and Fourth Medical Center of the Chinese PLA General Hospital, 100048, Beijing, People's Republic of China. c_ff@sina.com.ORCID 0000-0002-3564-4012
Chinese PLA General Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82130062
6 · The paper itself

Abstract

Tumor necrosis factor (TNF)-α-induced protein 8-like 2 (TIPE2) is a newly discovered negative immunoregulatory protein that is involved in various cellular immune responses to infections. However, the underlying mechanism by which TIPE2 affects the immune function of dendritic cells (DCs) is not yet understood. This study aimed to determine the correlations among DCs TIPE2 expression, autophagic activity and immune function in the context of sepsis. In addition, the signaling pathway by which TIPE2 regulates autophagy in DCs was investigated. We reported for the first time that TIPE2 overexpression (knock-in, KI) exerted an inhibitory effect on autophagy in DCs and markedly suppressed the immune function of DCs upon septic challenge both in vitro and in vivo. In addition, TIPE2 knockout (KO) in DCs significantly enhanced autophagy and improved the immune response of DCs in sepsis. Of note, we found that the transforming growth factor-β (TGF-β)-activated kinase-1 (TAK1)/c-Jun N-terminal kinase (JNK) pathway was inhibited by TIPE2 in DCs, resulting in downregulated autophagic activity. Collectively, these results suggest that TIPE2 can suppress the autophagic activity of DCs by inhibiting the TAK1/JNK signaling pathway and further negatively regulate the immune function of DCs in the development of septic complications.

Indexed as

AutophagyMAP Kinase Signaling SystemAnimalsAutophagosomesDendritic CellsDisease Models, AnimalDown-RegulationImmunityIntracellular Signaling Peptides and ProteinsLipopolysaccharidesMaleMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMiceMice, Inbred C57BLMice, KnockoutIntracellular Signaling Peptides and ProteinsLipopolysaccharidesMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesTIPE2 protein, mouse

Identifiers

PMID34718337
PMCPMC8557212
OpenAlexW3208806171

What Socratic 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 Socratic graph.