Evidence map›Paper›PMID 10770797›Full record

ArticleThe Journal of experimental medicine2000

Markedly different pathogenicity of four immunoglobulin G isotype-switch variants of an antierythrocyte autoantibody is based on their capacity to interact in vivo with the low-affinity Fcgamma receptor III.

L Fossati-Jimack, A Ioan-Facsinay, L Reininger, Y Chicheportiche, N Watanabe, T Saito, F M Hofhuis, J E Gessner, C Schiller, R E Schmidt and 3 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
11.7field-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

55 citing papers in PubMed, 179 citations in OpenAlex.

  1. Trial
  2. Article
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  5. Article
  6. CD4Vaccines · 2020
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Mechanisms of Autoantibody-Induced Pathology.Frontiers in immunology · 2017
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Critical role of NKT cells in posttransplant alloantibody production.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2014
    Article
  20. 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

13 authors at 6 institutions in 5 countries.

L Fossati-JimackDepartment of Pathology, University of Geneva, 1211 Geneva 4, Switzerland.
A Ioan-Facsinay
L Reininger
Y Chicheportiche
N Watanabe
T Saito
F M Hofhuis
J E Gessner
C Schiller
R E Schmidt
T Honjo
J S Verbeek
S Izui
Medizinische Hochschule Hannover · DEUniversity of Geneva · CHChiba University · JPLeiden University Medical Center · NLInserm · FRKyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Using three different Fcgamma receptor (FcgammaR)-deficient mouse strains, we examined the induction of autoimmune hemolytic anemia by each of the four immunoglobulin (Ig)G isotype-switch variants of a 4C8 IgM antierythrocyte autoantibody and its relation to the contributions of the two FcgammaR, FcgammaRI, and FcgammaRIII, operative in the phagocytosis of opsonized particles. We found that the four IgG isotypes of this antibody displayed striking differences in pathogenicity, which were related to their respective capacity to interact in vivo with the two phagocytic FcgammaRs, defined as follows: IgG2a > IgG2b > IgG3/IgG1 for FcgammaRI, and IgG2a > IgG1 > IgG2b > IgG3 for FcgammaRIII. Accordingly, the IgG2a autoantibody exhibited the highest pathogenicity, approximately 20-100-fold more potent than its IgG1 and IgG2b variants, respectively, while the IgG3 variant, which displays little interaction with these FcgammaRs, was not pathogenic at all. An unexpected critical role of the low-affinity FcgammaRIII was revealed by the use of two different IgG2a anti-red blood cell autoantibodies, which displayed a striking preferential utilization of FcgammaRIII, compared with the high-affinity FcgammaRI. This demonstration of the respective roles in vivo of four different IgG isotypes, and of two phagocytic FcgammaRs, in autoimmune hemolytic anemia highlights the major importance of the regulation of IgG isotype responses in autoantibody-mediated pathology and humoral immunity.

Indexed as

Anemia, Hemolytic, AutoimmuneAnimalsAutoantibodiesBase SequenceDNA PrimersErythrocytesGenetic VariationImmunoglobulin GImmunoglobulin IsotypesImmunoglobulin Switch RegionIn Vitro TechniquesIronLiverMiceMice, Inbred BALB CMice, Inbred C57BLAutoantibodiesDNA PrimersImmunoglobulin GImmunoglobulin IsotypesIronReceptors, IgG

Identifiers

PMID10770797
PMCPMC2193130
OpenAlexW2148706075

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.