Evidence map›Paper›PMID 33841441›Full record

ArticleFrontiers in immunology2021

A Novel Autoantibody Induced by Bacterial Biofilm Conserved Components Aggravates Lupus Nephritis.

Wenyan Fu, Yu Liu, Fangjie Liu, Chenghua Liu, Jingjing Li, Jiali Niu, Peng Han, Dan Xu, Jiaojiao Hou, Yuanfang Ma and 4 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 11 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 1 country.

Wenyan FuBeijing Institute of Pharmacology and Toxicology, Beijing, China.
Yu LiuBeijing Institute of Pharmacology and Toxicology, Beijing, China.
Fangjie LiuBeijing Institute of Pharmacology and Toxicology, Beijing, China.
Chenghua LiuBeijing Institute of Pharmacology and Toxicology, Beijing, China.
Jingjing LiJoint National Laboratory for Antibody Drug Engineering, Henan University, Kaifeng, China.
Jiali NiuJoint National Laboratory for Antibody Drug Engineering, Henan University, Kaifeng, China.
Peng HanDepartment of Rheumatology and Immunology, People's Hospital, Peking University, Beijing, China.
Dan XuDepartment of Rheumatology and Immunology, People's Hospital, Peking University, Beijing, China.
Jiaojiao HouJoint National Laboratory for Antibody Drug Engineering, Henan University, Kaifeng, China.
Yuanfang MaJoint National Laboratory for Antibody Drug Engineering, Henan University, Kaifeng, China.
Jiannan FengBeijing Institute of Pharmacology and Toxicology, Beijing, China.
Zhanguo LiDepartment of Rheumatology and Immunology, People's Hospital, Peking University, Beijing, China.
Rong MuDepartment of Rheumatology and Immunology, People's Hospital, Peking University, Beijing, China.
Guang YangBeijing Institute of Pharmacology and Toxicology, Beijing, China.
Henan University · CNPeking University People's Hospital · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with multiple autoantibody production and often affects the kidneys, known as lupus nephritis. However, the mechanism underlying lupus nephritis development is unclear. Biofilms that protect bacteria from stress are ubiquitous in almost every environment. Here, we identified that a conserved peptide (HU1) derived from DNABII proteins, one of major bacterial biofilm components, was specifically recognized by sera from about 47% patients with SLE. Moreover, the serum anti-HU1 levels showed a significant positive correlation with lupus nephritis occurrence. Presence of antibodies against HU1 in pristane-induced mice aggravated lupus nephritis, although these antibodies also attenuated bacterial biofilm formation. We further identified that antibodies against HU1 cross-recognized protein disulfide isomerase (P4HB) located on the renal cell surface and inhibited the activities of this enzyme. Our findings reveal a novel mechanism underlying the development of lupus nephritis triggered by bacterial biofilms.

Indexed as

BiofilmsAmino Acid SequenceAnimalsAntigens, BacterialAutoantibodiesAutoantigensBacteriaBiomarkersDisease Models, AnimalDisease ProgressionDisease SusceptibilityEnzyme-Linked Immunosorbent AssayFemaleFluorescent Antibody TechniqueHumansLupus Erythematosus, SystemicAntigens, BacterialAutoantibodiesAutoantigensBiomarkersPeptidespristaneTerpenesautoantibodybacterial biofilmDNABIIlupus nephritisprotein disulfide isomerase

Identifiers

PMID33841441
PMCPMC8027312
OpenAlexW3140606631

What OpenQuestion holds

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LicenceCC BY
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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.