Evidence map›Paper›PMID 20217455›Full record

ReviewCellular and molecular life sciences : CMLS2010

The neonatal Fc receptor as therapeutic target in IgG-mediated autoimmune diseases.

Alina Sesarman, Gestur Vidarsson, Cassian Sitaru

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06765161 (Efgartigimod in IVIG Dependent Myasthenia Gravis Patients), which is not on this map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.0field-weighted citation impact, top 10% 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.

NCT06765161 phase3recruitingnot on this mapstarted 2025, after this paper: background citation

Efgartigimod in IVIG Dependent Myasthenia Gravis Patients

TypeinterventionalSponsorClinique Neuro-OutaouaisRan2025 to 2027Enrolled30ConditionsMyasthaenia GravisArmsefgartigimod administration
3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 55 citations in OpenAlex.

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  16. In Vitro, Ex Vivo, and In Vivo Models for the Study of Pemphigus.International journal of molecular sciences · 2022
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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

3 authors at 2 institutions in 2 countries.

Alina SesarmanDepartment of Dermatology, University of Freiburg, Hauptstrasse 7, Freiburg, Germany.
Gestur Vidarsson
Cassian Sitaru
University of Freiburg · DESanquin · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Therapy approaches based on lowering levels of pathogenic autoantibodies represent rational, effective, and safe treatment modalities of autoimmune diseases. The neonatal Fc receptor (FcRn) is a major factor regulating the serum levels of IgG antibodies. While FcRn-mediated half-life extension is beneficial for IgG antibody responses against pathogens, it also prolongs the serum half-life of IgG autoantibodies and thus promotes tissue damage in autoimmune diseases. In the present review article, we examine current evidence on the relevance of FcRn in maintaining high autoantibody levels and discuss FcRn-targeted therapeutic approaches. Further investigation of the FcRn-IgG interaction will not only provide mechanistic insights into the receptor function, but should also greatly facilitate the design of therapeutics combining optimal pharmacokinetic properties with the appropriate antibody effector functions in autoimmune diseases.

Indexed as

AnimalsAntibodiesAutoantibodiesAutoimmune DiseasesHalf-LifeHistocompatibility Antigens Class IImmunoglobulin Fc FragmentsMiceRatsReceptors, FcSerumAntibodiesAutoantibodiesFc receptor, neonatalHistocompatibility Antigens Class IImmunoglobulin Fc FragmentsReceptors, Fc

Identifiers

PMID20217455
PMCPMC11115620
OpenAlexW2021197354

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.