Evidence map›Paper›PMID 38570836›Full record

ArticleCell communication and signaling : CCS2024

Gut microbiota-derived butyrate restores impaired regulatory T cells in patients with AChR myasthenia gravis via mTOR-mediated autophagy.

Long He, Zhuotai Zhong, Shuting Wen, Peiwu Li, Qilong Jiang, Fengbin Liu

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
9.2field-weighted citation impact, top 1% 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

25 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Harnessing the microbiome for cancer therapy.Nature reviews. Microbiology · 2026
    Review
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  4. Nutrients · 2026
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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

6 authors at 3 institutions in 1 country.

Long He *Department of Digestive Endoscopy, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.
Zhuotai Zhong *Department of Gastroenterology, Wangjing Hospital, China Academy of Chinese Medical Sciences, No. 6, Wangjing Zhonghuan South Road, Futong East Street, Chaoyang District, Beijing City, China.
Shuting WenDepartment of Gastroenterology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, No. 55, Inner Ring West Road, Panyu District, Guangzhou, Guangzhou, Guangdong Province, 511400, China.
Peiwu LiDepartment of Hepatobiliary, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, No. 16 Airport Road, Baiyun District, Guangzhou, Guangdong Province, 510405, China. doctorlipw@gzucm.edu.cn.
Qilong JiangDepartment of Myopathies, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, No. 16 Airport Road, Baiyun District, Guangzhou, Guangdong Province, 510405, China. jpllpzx@126.com.
Fengbin LiuDepartment of Hepatobiliary, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, No. 16 Airport Road, Baiyun District, Guangzhou, Guangdong Province, 510405, China. liufb163@gzucm.edu.cn.
Guangzhou University of Chinese Medicine · CNFirst Affiliated Hospital of Guangzhou University of Chinese Medicine · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

National Key Research and Development Program of China Grant No. 2022YFC3501302National Natural Science Foundation of China Grant No. 8190413Scientific Research Team Training Project of Guangzhou University of Chinese Medicine Grant No. 2021XK18
6 · The paper itself

Abstract

More than 80% of patients with myasthenia gravis (MG) are positive for anti-acetylcholine receptor (AChR) antibodies. Regulatory T cells (Tregs) suppress overproduction of these antibodies, and patients with AChR antibody-positive MG (AChR MG) exhibit impaired Treg function and reduced Treg numbers. The gut microbiota and their metabolites play a crucial role in maintaining Treg differentiation and function. However, whether impaired Tregs correlate with gut microbiota activity in patients with AChR MG remains unknown. Here, we demonstrate that butyric acid-producing gut bacteria and serum butyric acid level are reduced in patients with AChR MG. Butyrate supplementation effectively enhanced Treg differentiation and their suppressive function of AChR MG. Mechanistically, butyrate activates autophagy of Treg cells by inhibiting the mammalian target of rapamycin. Activation of autophagy increased oxidative phosphorylation and surface expression of cytotoxic T-lymphocyte-associated protein 4 on Treg cells, thereby promoting Treg differentiation and their suppressive function in AChR MG. This observed effect of butyrate was blocked using chloroquine, an autophagy inhibitor, suggesting the vital role of butyrate-activated autophagy in Tregs of patients with AChR MG. We propose that gut bacteria derived butyrate has potential therapeutic efficacy against AChR MG by restoring impaired Tregs.

Indexed as

Gastrointestinal MicrobiomeMyasthenia GravisAutoantibodiesButyric AcidHumansReceptors, CholinergicT-Lymphocytes, RegulatoryAutoantibodiesButyric AcidReceptors, CholinergicAutophagyButyrateGut microbiotaMyasthenia gravisTreg

Identifiers

PMID38570836
PMCPMC10988943
OpenAlexW4393864737

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.