Evidence map›Paper›PMID 40289872›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Microbiota-Derived Inosine Suppresses Systemic Autoimmunity via Restriction of B Cell Differentiation and Migration.

Lingyu Gao, Yuhan Zhang, Zhi Hu, Shengwen Chen, Qiaolin Wang, Yong Zeng, Huiqi Yin, Junpeng Zhao, Yijing Zhan, Changxing Gao and 6 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

20 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. A metabolomic signatures in hyperuricemia: a systematic review.Metabolomics : Official journal of the Metabolomic Society · 2026
    Pooled it
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  14. Microbiota-gut-kidney axis in health and renal disease.International journal of biological sciences · 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

16 authors.

Lingyu GaoHospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, 210042, China.
Yuhan ZhangHospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, 210042, China.
Zhi HuHospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, 210042, China.
Shengwen ChenHospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, 210042, China.
Qiaolin WangHospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, 210042, China.
Yong ZengHunan Key Laboratory of Medical Epigenomics, The Second Xiangya Hospital, Central South University, Changsha, 410013, China.
Huiqi YinHospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, 210042, China.
Junpeng ZhaoHospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, 210042, China.
Yijing ZhanHospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, 210042, China.
Changxing GaoHospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, 210042, China.
Yue XinHospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, 210042, China.
Bing ChenClinical Laboratory, The Second Hospital of Anhui Medical University, Hefei, 230601, China.
Stijn van der VeenDepartment of Microbiology, and Department of Dermatology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310058, China.
Ming ZhaoHospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, 210042, China.
Deyu FangDepartment of Pathology, Northwestern University Feinberg School of Medicine, Chicago, IL, 60611, USA.
Qianjin LuHospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, 210042, China.ORCID https://orcid.org/0000-0002-7749-9618

Funding

CAMS Innovation Fund for Medical Sciences (CIFMS) No 2021-I2M-1-059CAMS Innovation Fund for Medical Sciences (CIFMS) No 2024-I2M-ZH-020Key Program of the National Natural Science Foundation of China NO.82430102National Key R&D Program of China 2022YFC3601800National Natural Science Foundation of China 82404154Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences 2020-RC320-003Special Program of National Natural Science Foundation of China 32141004
6 · The paper itself

Abstract

The role of gut microbiota dysbiosis in systemic lupus erythematosus (SLE) pathogenesis remains elusive. Here, it is shown that fecal microbiota transplantation (FMT) from healthy mice to lupus mice ameliorates lupus-like symptoms. Microbiota reconstitution effectively reduces systemic class switch recombination (CSR) and elevates immunoglobulin heavy chain (IGH) naïve isotype. Microbiota profiling reveals an enrichment of Lactobacillus johnsonii post-FMT, with a significant correlation to purine metabolites. Importantly, the L. johnsonii-derived inosine, an intermediate metabolite in purine metabolism, effectively alleviates lupus pathogenesis in mice. Inosine inhibits B cell differentiation and reduces renal B cell infiltration to protect mice from lupus. At the molecular level, inosine reprograms B cells through the extracellular signal-regulated kinase (ERK)-hypoxia-inducible factor-1alpha (HIF-1α) signaling pathway. Therefore, this study highlights the discovery of a novel microbial metabolite modulating autoimmunity and suggests its potential for innovative microbiome-based therapeutic approaches.

Indexed as

AutoimmunityB-LymphocytesCell DifferentiationGastrointestinal MicrobiomeInosineLupus Erythematosus, SystemicAnimalsCell MovementDisease Models, AnimalDysbiosisFecal Microbiota TransplantationFemaleMiceMice, Inbred C57BLInosineB cell differentiationB cell migrationfecal microbiota transplantation (FMT)inosineLactobacillus johnsoniilupus nephritis (LN)purine metabolitessystemic lupus erythematosus (SLE)

Identifiers

PMID40289872
PMCPMC12120789

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.