Evidence map›Paper›PMID 6350525›Full record

ArticleThe Journal of experimental medicine1983

Induction of rheumatoid antibodies in the mouse. Regulated production of autoantibody in the secondary humoral response.

D A Nemazee, V L Sato

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1983. 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
8.7field-weighted citation impact, top 2% 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, 137 citations in OpenAlex.

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  7. Peripheral deletion of rheumatoid factor B cells after abortive activation by IgG.Proceedings of the National Academy of Sciences of the United States of America · 1997
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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

2 authors.

D A Nemazee
V L Sato

Funding

Training in Molecular, Cellular, and Chemical BiologyT32GM007598 · NIGMS · HARVARD UNIVERSITY · PI DULAC, CATHERINE · 1985 to 2019
$16.2M
NCI NIH HHS CA24368NIGMS NIH HHS 5T32GM07598
6 · The paper itself

Abstract

A/J mice were found to produce autoreactive IgM anti-IgG1 in response to secondary immunization with a number of protein antigens. No anti-IgG1 was produced after a single such immunization, indicating that antigen: IgG1 antibody complexes were responsible for inducing the autoreactive response. The size of the anti-IgG1 response was in some cases massive and of the same order of magnitude as the response to the foreign immunizing material. No significant anti-IgG2a, anti-IgG2b, or anti-IgG3 response was found in mice producing anti-IgG1. Virtually all of the anti-IgG1 material produced was of the IgM class and bound to the Fc region of autologous IgG1. A component of the anti-IgG1 was shown to be able to distinguish between the two mouse IgG1 allotypes. These results suggest that self-reactive anti-IgG is a common component of the secondary immune response of mice that may have powerful physiological and immunoregulatory effects.

Indexed as

Immunization, SecondaryAnimalsAntibody-Producing CellsAntibody SpecificityAutoimmune DiseasesBinding Sites, AntibodyHaptensHemolytic Plaque TechniqueImmunoglobulin AllotypesImmunoglobulin GImmunoglobulin MMiceMice, Inbred AMice, Inbred BALB CMice, Inbred C57BLRheumatoid FactorHaptensImmunoglobulin AllotypesImmunoglobulin GImmunoglobulin MRheumatoid Factor

Identifiers

PMID6350525
PMCPMC2187336
OpenAlexW2095935128

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.