Evidence map›Paper›PMID 9824476›Full record

ArticleImmunology1998

Anti-DNA IgA autoantibodies are spontaneously generated in mouse Peyer's patches.

M Shimoda, Y Inoue, A Ametani, J Fujiwara, N M Tsuji, J Kurisaki, N Azuma, C Kanno

Open access · greenAbstract read
In one paragraph

Article in Immunology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

1 citing paper in PubMed, 10 citations in OpenAlex.

  1. Article
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

8 authors at 4 institutions in 2 countries.

M ShimodaDepartment of Applied Biochemistry, Utsunomiya University, Utsunomiya, Tochigi.
Y Inoue
A Ametani
J Fujiwara
N M Tsuji
J Kurisaki
N Azuma
C Kanno
Utsunomiya University · JPNational Institute of Animal Health · JPAisin (Japan) · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IgA antibodies in the mucosal immune system are produced specifically to environmental antigens such as virus and bacteria, and possibly to some food components, which will provide a potential luminal antigen, DNA. To study the immune response to DNA in the gut, we established B-cell hybridomas producing IgA monoclonal antibodies (mAb) from Peyer's patches (PP) of non-immunized, non-autoimmune, specific pathogen-free BALB/c mice, and examined their specificity by enzyme-linked immunosorbent assay (ELISA). Three mAb out of 18 bound strongly to self, bacterial and synthetic DNA, with Kd of about 10-7 m. One of the three mAb also reacted with the histone component and another reacted with some mouse food component. The VH genes of these three mAb have not previously been reported to have anti-DNA specificity, and carry putative somatically mutated sites favouring DNA binding in CDR. The features resemble those of anti-DNA antibodies found in human and murine models of systemic lupus erythmatosus (SLE), and are indicative of an antigen-driven selection process. Our findings suggest that even in normal healthy animals, anti-DNA antibodies of IgA isotype can be produced in certain peripheral environments such as in PP by spontaneous antigenic stimulation.

Indexed as

Amino Acid SequenceAnimalsAntibodies, AntinuclearAntibodies, MonoclonalBase SequenceB-LymphocytesDNAEnzyme-Linked Immunosorbent AssayFemaleHybridomasImmunoglobulin AMiceMice, Inbred BALB CMolecular Sequence DataMutationPeyer's PatchesAntibodies, AntinuclearAntibodies, MonoclonalDNAImmunoglobulin A

Identifiers

PMID9824476
PMCPMC1364305
OpenAlexW2029641329

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.