Evidence map›Paper›PMID 32896308›Full record

ReviewThe Journal of allergy and clinical immunology2020

Targeting FcRn for immunomodulation: Benefits, risks, and practical considerations.

Hans-Hartmut Peter, Hans D Ochs, Charlotte Cunningham-Rundles, Donald C Vinh, Peter Kiessling, Bernhard Greve, Stephen Jolles

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of allergy and clinical immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 3% 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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 115 citations in OpenAlex.

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  14. Targeting FcRn for immunomodulation: a promising therapy in autoimmune inflammatory rheumatic diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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23 more citing papers are in PubMed but not listed here.

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

7 authors at 6 institutions in 4 countries.

Hans-Hartmut PeterFreiburg University Hospital, Centre for Chronic Immunodeficiency, Freiburg, Germany.
Hans D OchsSeattle Children's Research Institute, Seattle, Wash; Department of Pediatrics, University of Washington, Seattle, Wash.
Charlotte Cunningham-RundlesDivision of Clinical Immunology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY.
Donald C VinhDivision of Infectious Diseases, Department of Medicine and Department of Medical Microbiology, McGill University Health Centre, Montreal, Quebec, Canada; Infectious Diseases & Immunity in Global Health Program, Research Institute-McGill University Health Centre, Montreal, Quebec, Canada.
Peter KiesslingUCB Pharma, Monheim-am-Rhein, Germany.
Bernhard GreveUCB Pharma, Monheim-am-Rhein, Germany.
Stephen JollesImmunodeficiency Centre for Wales, University Hospital of Wales, Cardiff, United Kingdom. Electronic address: jollessr@cardiff.ac.uk.
UCB Pharma (Germany) · DEIcahn School of Medicine at Mount Sinai · USMcGill University Health Centre · CAUniversity Hospital of Wales · GBUniversity Medical Center Freiburg · DEUniversity of Washington · US

Funding

Regulation of IgA class switching in the intestinal mucosaP01AI061093 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI CUNNINGHAM-RUNDLES, CHARLOTTE · 2004 to 2021
$29.8M
NIAID NIH HHS P01 AI061093
6 · The paper itself

Abstract

The neonatal fragment crystallizable (Fc) receptor (FcRn) functions as a recycling mechanism to prevent degradation and extend the half-life of IgG and albumin in the circulation. Several FcRn inhibitors selectively targeting IgG recycling are now moving rapidly toward clinical practice in neurology and hematology. These molecules accelerate the destruction of IgG, reducing pathogenic IgG and IgG immune complexes, with no anticipated effects on IgA, IgM, IgE, complement, plasma cells, B cells, or other cells of the innate or adaptive immune systems. FcRn inhibitors have potential for future use in a much wider variety of antibody-mediated autoimmune diseases. Given the imminent clinical use, potential for broader utility, and novel mechanism of action of FcRn inhibitors, here we review data from 4 main sources: (a) currently available activity, safety, and mechanism-of-action data from clinical trials of FcRn inhibitors; (b) other procedures and treatments that also remove IgG (plasma donation, plasma exchange, immunoadsorption); (c) diseases resulting in loss of IgG; and (d) primary immunodeficiencies with potential mechanistic similarities to those induced by FcRn inhibitors. These data have been evaluated to provide practical considerations for the assessment, monitoring, and reduction of any potential infection risk associated with FcRn inhibition, in addition to highlighting areas for future research.

Indexed as

Antibodies, BlockingAntibodies, MonoclonalAutoantibodiesAutoimmune DiseasesDrug-Related Side Effects and Adverse ReactionsHistocompatibility Antigens Class IHumansImmunomodulationMolecular Targeted TherapyPractice Guidelines as TopicReceptors, FcRiskRisk AssessmentAntibodies, BlockingAntibodies, MonoclonalAutoantibodiesFc receptor, neonatalHistocompatibility Antigens Class IReceptors, Fcalbuminantibody-mediated autoimmunityautoantibodyFcRnFcRn inhibitorshypogammaglobulinemiaIgGimmunoglobulininfection riskneonatal Fc receptor

Identifiers

PMID32896308
PMCPMC7471860
OpenAlexW3083023871

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.