Evidence map›Paper›PMID 36982860›Full record

ReviewInternational journal of molecular sciences2023

Physiological and Pathophysiological Roles of IgM Fc Receptor (FcµR) Isoforms.

Hiromi Kubagawa, Caren Clark, Christopher M Skopnik, Pedram Mahmoudi Aliabadi, Khlowd Al-Qaisi, Ruth Teuber, Peter K Jani, Andreas Radbruch, Fritz Melchers, Niklas Engels and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
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

11 authors at 2 institutions in 1 country.

Hiromi KubagawaDeutsches Rheuma-Forschungszentrum, 10117 Berlin, Germany.
Caren ClarkInstitute of Cellular & Molecular Immunology, University Medical Center, 37073 Göttingen, Germany.
Christopher M SkopnikDeutsches Rheuma-Forschungszentrum, 10117 Berlin, Germany.ORCID 0000-0002-6089-4769
Pedram Mahmoudi AliabadiDeutsches Rheuma-Forschungszentrum, 10117 Berlin, Germany.
Khlowd Al-QaisiDeutsches Rheuma-Forschungszentrum, 10117 Berlin, Germany.
Ruth TeuberDeutsches Rheuma-Forschungszentrum, 10117 Berlin, Germany.
Peter K JaniDeutsches Rheuma-Forschungszentrum, 10117 Berlin, Germany.
Andreas RadbruchDeutsches Rheuma-Forschungszentrum, 10117 Berlin, Germany.ORCID 0000-0001-5753-0000
Fritz MelchersDeutsches Rheuma-Forschungszentrum, 10117 Berlin, Germany.
Niklas EngelsInstitute of Cellular & Molecular Immunology, University Medical Center, 37073 Göttingen, Germany.
Jürgen WienandsInstitute of Cellular & Molecular Immunology, University Medical Center, 37073 Göttingen, Germany.ORCID 0000-0001-8278-7668
German Rheumatism Research Centre · DEUniversity of Göttingen · DE

Funding

Leibniz Collaborative Excellence Grant CHROQ-K121/2018
6 · The paper itself

Abstract

IgM is the first antibody to emerge during phylogeny, ontogeny, and immune responses and serves as a first line of defense. Effector proteins interacting with the Fc portion of IgM, such as complement and its receptors, have been extensively studied for their functions. IgM Fc receptor (FcµR), identified in 2009, is the newest member of the FcR family and is intriguingly expressed by lymphocytes only, suggesting the existence of distinct functions as compared to the FcRs for switched Ig isotypes, which are expressed by various immune and non-hematopoietic cells as central mediators of antibody-triggered responses by coupling the adaptive and innate immune responses. Results from FcµR-deficient mice suggest a regulatory function of FcµR in B cell tolerance, as evidenced by their propensity to produce autoantibodies of both IgM and IgG isotypes. In this article, we discuss conflicting views about the cellular distribution and potential functions of FcµR. The signaling function of the Ig-tail tyrosine-like motif in the FcµR cytoplasmic domain is now formally shown by substitutional experiments with the IgG2 B cell receptor. The potential adaptor protein associating with FcµR and the potential cleavage of its C-terminal cytoplasmic tail after IgM binding are still enigmatic. Critical amino acid residues in the Ig-like domain of FcµR for interacting with the IgM Cµ4 domain and the mode of interaction are now defined by crystallographic and cryo-electron microscopic analyses. Some discrepancies on these interactions are discussed. Finally, elevated levels of a soluble FcµR isoform in serum samples are described as the consequence of persistent B cell receptor stimulation, as seen in chronic lymphocytic leukemia and probably in antibody-mediated autoimmune disorders.

Indexed as

Receptors, Antigen, B-CellReceptors, FcAnimalsImmunoglobulin MMiceProtein IsoformsImmunoglobulin Mimmunoglobulin M receptorProtein IsoformsReceptors, Antigen, B-CellReceptors, Fcautoimmune diseaseschronic lymphocytic leukemia (CLL)Ig-tail tyrosine (ITT) motifsingle-cell RNA sequence (scRNAseq)soluble FcµR

Identifiers

PMID36982860
PMCPMC10058298
OpenAlexW4327969288

What OpenQuestion holds

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LicenceCC BY
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.