Evidence map›Paper›PMID 36426942›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2022

Mechanism of CD79A and CD79B Support for IgM+ B Cell Fitness through B Cell Receptor Surface Expression.

Kanutte Huse, Baoyan Bai, Vera I Hilden, Lise K Bollum, Thea K Våtsveen, Ludvig A Munthe, Erlend B Smeland, Jonathan M Irish, Sébastien Wälchli, June H Myklebust

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
5.3field-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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

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  20. Epstein-Barr virus BALF0/1 subverts the Caveolin and ERAD pathways to target B cell receptor complexes for degradation.Proceedings of the National Academy of Sciences of the United States of America · 2025
    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

10 authors at 2 institutions in 2 countries.

Kanutte HuseDepartment of Cancer Immunology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.ORCID 0000-0001-9128-670X
Baoyan BaiDepartment of Cancer Immunology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Vera I HildenDepartment of Cancer Immunology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Lise K BollumDepartment of Cancer Immunology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Thea K VåtsveenK.G. Jebsen Centre for B Cell Malignancies, Institute of Clinical Medicine, University of Oslo, Oslo, Norway.ORCID 0000-0002-4158-0617
Ludvig A MuntheK.G. Jebsen Centre for B Cell Malignancies, Institute of Clinical Medicine, University of Oslo, Oslo, Norway.ORCID 0000-0002-0344-3654
Erlend B SmelandDepartment of Cancer Immunology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Jonathan M IrishDepartment of Cell and Developmental Biology, Vanderbilt University, Nashville, TN.ORCID 0000-0001-9428-8866
Sébastien WälchliTranslational Research Unit, Section for Cellular Therapy, Department of Cancer Treatment, Oslo University Hospital, Oslo, Norway.ORCID 0000-0001-5869-1746
June H MyklebustDepartment of Cancer Immunology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway.
Oslo University Hospital · NOVanderbilt University · US

Funding

Single Cell Methods for Bioeffector Discovery and AnalysisR01CA226833 · NCI · VANDERBILT UNIVERSITY · PI BRIAN O BACHMANN, Jonathan Michael Irish · 2019 to 2026
$6.1M
NCI NIH HHS R01 CA226833
6 · The paper itself

Abstract

The BCR consists of surface-bound Ig and a heterodimeric signaling unit comprised of CD79A and CD79B. Upon cognate Ag recognition, the receptor initiates important signals for B cell development and function. The receptor also conveys Ag-independent survival signals termed tonic signaling. Although the requirement of a CD79A/CD79B heterodimer for BCR complex assembly and surface expression is well established based on mice models, few studies have investigated this in human mature B cells. In this study, we found that human tonsillar B cells with high surface expression of IgM or IgG had potentiated BCR signaling compared with BCRlow cells, and high IgM expression in germinal center B cells was associated with reduced apoptosis. We explored the mechanism for IgM surface expression by CRISPR/Cas9-induced deletion of CD79A or CD79B in four B lymphoma cell lines. Deletion of either CD79 protein caused loss of surface IgM in all cell lines and reduced fitness in three. From two cell lines, we generated stable CD79A or CD79B knockout clones and demonstrated that loss of CD79A or CD79B caused a block in N-glycan maturation and accumulation of immature proteins, compatible with retention of BCR components in the endoplasmic reticulum. Rescue experiments with CD79B wild-type restored surface expression of CD79A and IgM with mature glycosylation, whereas a naturally occurring CD79B G137S mutant disrupting CD79A/CD79B heterodimerization did not. Our study highlights that CD79A and CD79B are required for surface IgM expression in human B cells and illuminates the importance of the IgM expression level for signaling and fitness.

Indexed as

B-LymphocytesReceptors, Antigen, B-CellAnimalsCD79 AntigensCell CountGerminal CenterHumansImmunoglobulin MMiceCD79 AntigensCD79A protein, humanCD79B protein, humanImmunoglobulin MReceptors, Antigen, B-Cell

Identifiers

PMID36426942
PMCPMC9643646
OpenAlexW4304480073

What OpenQuestion holds

Textmetadata
LicenceTDM
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.