Evidence map›Paper›PMID 34434193›Full record

ArticleFrontiers in immunology2021

Primary Immune Responses and Affinity Maturation Are Controlled by IgD.

Timm Amendt, Omar El Ayoubi, Alexandra T Linder, Gabriele Allies, Marc Young, Corinna S Setz, Hassan Jumaa

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

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  11. TLR7 and IgM: Dangerous Partners in Autoimmunity.Antibodies (Basel, Switzerland) · 2023
    Review
  12. Article
  13. Review
  14. Article
  15. Autoreactive antibodies control blood glucose by regulating insulin homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  16. 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

7 authors at 1 institution in 1 country.

Timm AmendtInstitute of Immunology, Ulm University Medical Center, Ulm, Germany.
Omar El AyoubiInstitute of Immunology, Ulm University Medical Center, Ulm, Germany.
Alexandra T LinderInstitute of Immunology, Ulm University Medical Center, Ulm, Germany.
Gabriele AlliesInstitute of Immunology, Ulm University Medical Center, Ulm, Germany.
Marc YoungInstitute of Immunology, Ulm University Medical Center, Ulm, Germany.
Corinna S SetzInstitute of Immunology, Ulm University Medical Center, Ulm, Germany.
Hassan JumaaInstitute of Immunology, Ulm University Medical Center, Ulm, Germany.
Universität Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mature B cells co-express IgM and IgD B cell antigen receptors (BCR) on their surface. While IgM BCR expression is already essential at early stages of development, the role of the IgD-class BCR remains unclear as most B cell functions appeared unchanged in IgD-deficient mice. Here, we show that IgD-deficient mice have an accelerated rate of B cell responsiveness as they activate antibody production within 24h after immunization, whereas wildtype (WT) animals required 3 days to activate primary antibody responses. Strikingly, soluble monovalent antigen suppresses IgG antibody production induced by multivalent antigen in WT mice. In contrast, IgD-deficient mice were not able to modulate IgG responses suggesting that IgD controls the activation rate of B cells and subsequent antibody production by sensing and distinguishing antigen-valences. Using an insulin-derived peptide we tested the role of IgD in autoimmunity. We show that primary autoreactive antibody responses are generated in WT and in IgD-deficient mice. However, insulin-specific autoantibodies were detected earlier and caused more severe symptoms of autoimmune diabetes in IgD-deficient mice as compared to WT mice. The rapid control of autoimmune diabetes in WT animals was associated with the generation of high-affinity IgM that protects insulin from autoimmune degradation. In IgD-deficient mice, however, the generation of high-affinity protective IgM is delayed resulting in prolonged autoimmune diabetes. Our data suggest that IgD is required for the transition from primary, highly autoreactive, to secondary antigen-specific antibody responses generated by affinity maturation.

Indexed as

Antibody AffinityAntibody FormationAnimalsAutoantigensAutoimmunityB-LymphocytesFemaleImmunoglobulin DImmunoglobulin GLymphocyte ActivationMiceMice, Inbred C57BLReceptors, Antigen, B-CellAutoantigensImmunoglobulin DImmunoglobulin GReceptors, Antigen, B-Cellantigen-valencyautoimmunityB cell selectionIgDIgMtolerance

Identifiers

PMID34434193
PMCPMC8381280
OpenAlexW3187127926

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.