Evidence map›Paper›PMID 27039179›Full record

ReviewJournal of clinical immunology2016

The FcγR/IgG Interaction as Target for the Treatment of Autoimmune Diseases.

Peter Sondermann

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of clinical immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–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

11 citing papers in PubMed.

  1. Article
  2. Article
  3. Novel Therapies to Address Unmet Needs in ITP.Pharmaceuticals (Basel, Switzerland) · 2022
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Mechanisms of Autoantibody-Induced Pathology.Frontiers in immunology · 2017
    Review
  11. Ins and Outs of Antibodies.Journal of clinical immunology · 2016
    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

1 author.

Peter SondermannSuppreMol GmbH, Am Klopferspitz 19a, Martinsried, D-82152, Germany. peter.sondermann@baxalta.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

FcγRs are a crucial component of the antibody response as they mediate the cellular effector functions in response to IgG-containing immune complexes (ICs). Therefore, they also play a central role in the pathogenesis of autoimmune diseases which offers an attractive option to specifically target this class of molecules and their interaction with IgG for treatment of immune disorders. In detail, two strategies are discussed in this article. SM101, a soluble FcγR that is already in clinical development competes with the interaction of IgG with membrane FcγRs. Oppositely, SM201 recruits the inhibitory FcγRIIB for a broad down-modulation of the immune system. The presented approaches for the treatment of autoimmune diseases have the potential be more efficacious with fewer side effects than the currently used therapeutic options.

Indexed as

AnimalsAntigen-Antibody ComplexAutoimmune DiseasesHumansImmunoglobulin GImmunomodulationImmunosuppression TherapyMolecular Targeted TherapyProtein BindingReceptors, IgGAntigen-Antibody ComplexImmunoglobulin GReceptors, IgGFc-gamma receptorFcγRFcγRIIBIgGSM101SM201soluble FcγR

Identifiers

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.