Evidence map›Paper›PMID 29297752›Full record

ArticleAutophagy2018

IL4 (interleukin 4) induces autophagy in B cells leading to exacerbated asthma.

Fucan Xia, Changwen Deng, Yanyan Jiang, Yulan Qu, Jiewen Deng, Zhijian Cai, Yuanyuan Ding, Zhenhong Guo, Jianli Wang

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 84 citations in OpenAlex.

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  17. Autophagy in asthma and chronic obstructive pulmonary disease.Clinical science (London, England : 1979) · 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

9 authors at 4 institutions in 1 country.

Fucan Xiaa Institute of Immunology , Zhejiang University School of Medicine , Hangzhou , China.
Changwen Dengb Department of Respiratory Medicine , Changhai Hospital , Second Military Medical University , Shanghai , China.
Yanyan Jiangc National Key Laboratory of Medical Immunology & Institute of Immunology , Second Military Medical University , Shanghai , China.
Yulan Qub Department of Respiratory Medicine , Changhai Hospital , Second Military Medical University , Shanghai , China.
Jiewen Dengc National Key Laboratory of Medical Immunology & Institute of Immunology , Second Military Medical University , Shanghai , China.
Zhijian Caia Institute of Immunology , Zhejiang University School of Medicine , Hangzhou , China.
Yuanyuan Dingd National Key Laboratory of Medical Molecular Biology & Department of Immunology , Institute of Basic Medical Sciences , Peking Union Medical College , Chinese Academy of Medical Sciences , Beijing , China.
Zhenhong Guoc National Key Laboratory of Medical Immunology & Institute of Immunology , Second Military Medical University , Shanghai , China.
Jianli Wanga Institute of Immunology , Zhejiang University School of Medicine , Hangzhou , China.
Second Military Medical University · CNZhejiang University · CNChanghai Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Allergic asthma is a common airway inflammatory disease in which B cells play important roles through IgE production and antigen presentation. SNP (single nucleotide polymorphism) analysis showed that Atg (autophagy-related) allele mutations are involved in asthma. It has been demonstrated that macroautophagy/autophagy is essential for B cell survival, plasma cell differentiation and immunological memory maintenance. However, whether B cell autophagy participates in asthma pathogenesis remains to be investigated. In this report, we found that autophagy was enhanced in pulmonary B cells from asthma-prone mice. Autophagy deficiency in B cells led to attenuated immunopathological symptoms in asthma-prone mice. Further investigation showed that IL4 (interleukin 4), a key effector Th2 cytokine in allergic asthma, was critical for autophagy induction in B cells both in vivo and in vitro, which further sustained B cell survival and enhanced antigen presentation by B cells. Moreover, IL4-induced autophagy depended on JAK signaling via an MTOR-independent, PtdIns3K-dependent pathway. Together, our data indicate that B cell autophagy aggravates experimental asthma through multiple mechanisms.

Indexed as

AllelesAnimalsAsthmaAutophagyB-LymphocytesCytokinesHumansInterleukin-4Mice, Inbred C57BLPolymorphism, Single NucleotideCytokinesIL4 protein, humanInterleukin-4Antigen presentationasthmaautophagyB cellIL4

Identifiers

PMID29297752
PMCPMC5915013
OpenAlexW2782355556

What OpenQuestion holds

Textmetadata
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.