Evidence map›Paper›PMID 34001658›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2021

Cutting Edge: Myosin 18A Is a Novel Checkpoint Regulator in B Cell Differentiation and Antibody-Mediated Immunity.

Michael B Cheung, Gospel Enyindah-Asonye, Ken Matsui, Ivan Kosik, Nina Dvorina, William M Baldwin, Jonathan W Yewdell, Neetu Gupta

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 40% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Michael B CheungDepartment of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, OH; and.ORCID 0000-0002-0021-3802
Gospel Enyindah-AsonyeDepartment of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, OH; and.
Ken MatsuiDepartment of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, OH; and.
Ivan KosikLaboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.
Nina DvorinaDepartment of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, OH; and.
William M BaldwinDepartment of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, OH; and.
Jonathan W YewdellLaboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.ORCID 0000-0002-3826-1906
Neetu GuptaDepartment of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, OH; and guptan@ccf.org.
Cleveland Clinic Lerner College of Medicine · USNational Institutes of Health · US

Funding

Immunobiology and Virology of Influenza A VirusZIAAI001211 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI YEWDELL, JONATHAN W · 2016 to 2025
$10.4M
Regulation of B cell activation in lupusR01AR067705 · NIAMS · CLEVELAND CLINIC LERNER COM-CWRU · PI GUPTA, NEETU · 2016 to 2020
$1.9M
Novel unconventional myosins in B cell activationR21AI117350 · NIAID · CLEVELAND CLINIC LERNER COM-CWRU · PI GUPTA, NEETU · 2016 to 2017
$436k
NIAID NIH HHS R21 AI117350NIAMS NIH HHS R01 AR067705
6 · The paper itself

Abstract

We investigated the function of the newly discovered myosin family protein myosin 18A (Myo18A) in Ab-mediated immunity by generating B cell-conditional Myo18A-deficient mice. Myo18A deficiency led to expansion of bone marrow progenitor B cells and mature B cells in secondary lymphoid organs. Myo18A-deficient mice displayed serum IgM hyperglobulinemia and increased splenic IgM-secreting cells, with older mice switching to IgG1 hyperglobulinemia and autoantibody development. Immunization of Myo18A-deficient mice with inactivated influenza virus led to development of more potent neutralizing Abs against the major Ag hemagglutinin, associated with persistent accumulation of Ag-specific germinal center B cells and more Ag-specific bone marrow plasma cells. In vitro stimulation with TLR7 and BCR ligands revealed a greater ability of Myo18A-deficient B cells to differentiate into Ab-secreting cells, associated with higher AID and Blimp-1 expression. Overall, our study demonstrates that Myo18A is a novel negative regulator of B cell homeostasis, differentiation, and humoral immunity.

Indexed as

AnimalsAntibodies, MonoclonalB-LymphocytesCell DifferentiationFemaleImmunity, HumoralMaleMiceMice, KnockoutMice, TransgenicMyosinsAntibodies, MonoclonalMyo18a protein, mouseMyosins

Identifiers

PMID34001658
PMCPMC8165029
OpenAlexW3162470932

What OpenQuestion holds

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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.