Evidence map›Paper›PMID 24442430›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

CD19 and CD32b differentially regulate human B cell responsiveness.

Jodi L Karnell, Nazzareno Dimasi, Fredrick G Karnell, Ryan Fleming, Ellen Kuta, Mildred Wilson, Herren Wu, Changshou Gao, Ronald Herbst, Rachel Ettinger

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

33 citing papers in PubMed, 50 citations in OpenAlex.

  1. Trial
  2. Trial
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  4. Article
  5. Article
  6. Induced proximity at the cell surface.Nature biotechnology · 2025
    Review
  7. Article
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  10. Article
  11. Article
  12. Article
  13. CIDP: Analysis of Immunomarkers During COVID-19 mRNA-Vaccination and IVIg-Immunomodulation: An Exploratory Study.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023
    Article
  14. Article
  15. Review
  16. Comprehensive phenotyping of human peripheral blood B lymphocytes in healthy conditions.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2022
    Review
  17. Article
  18. Article
  19. Review
  20. Abundance and Expression of Shiga Toxin Genes inFrontiers in cellular and infection microbiology · 2021
    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 3 institutions in 3 countries.

Jodi L KarnellRespiratory, Inflammation, and Autoimmunity Group, MedImmune, LLC, Gaithersburg, MD 20878;
Nazzareno Dimasi
Fredrick G Karnell
Ryan Fleming
Ellen Kuta
Mildred Wilson
Herren Wu
Changshou Gao
Ronald Herbst
Rachel Ettinger
Institute of Neuroimmunology of the Slovak Academy of Sciences · SKAstraZeneca (Germany) · DENational Institutes of Health · US

Funding

Intramural NIH HHS Z99 AR999999
6 · The paper itself

Abstract

B cell activation is regulated by a variety of signals. CD19 positively regulates B cell activation, augmenting signals delivered through the BCR complex. In contrast, CD32b contains an ITIM and negatively regulates BCR signaling. Importantly, there are drugs currently in clinical trials and preclinical development that cross-link CD32b to molecules within the BCR complex. We wanted to address how single engagement versus cotargeting these molecules affects human B cell function. When B cells from healthy individuals were activated by signals that mimic a T cell response (IL-21 costimulation), ligation of CD32b, but not CD19, inhibited B cell expansion and plasma cell (PC) differentiation. In contrast, when B cells were activated through TLR, anti-CD19, but not anti-CD32b, blunted the response. However, when both CD19 and CD32b were coengaged by a bispecific anti-CD19×CD32b Ab, both types of stimuli were potently inhibited. Cross-linking CD19 with CD32b also inhibited Ab-independent functions of B cells, such as HLA upregulation, cytokine production, and the ability of B cells to prime CD4(+) T cells. Finally, although cross-linking CD19 and CD32b inhibited PC differentiation of primary B cells, it did not alter Ig production from pre-established PCs. These data elucidate the mechanism by which a complex set of signals determines the fate of B cell responsiveness. Although signals through CD19 influence TLR-driven activation, CD32b impacts the magnitude of the response following IL-21 costimulation. Therefore, simultaneous targeting of multiple surface molecules may be a necessary approach to comprehensively modulate B cell activation in vivo.

Indexed as

AntibodiesAntigens, CD19Antigens, Differentiation, B-LymphocyteAutoimmune DiseasesB-LymphocytesCD4-Positive T-LymphocytesCell DeathCell DifferentiationCells, CulturedCross-Linking ReagentsHumansImmunologic MemoryInterleukin-21InterleukinsLymphocyte ActivationPlasma CellsAntibodiesAntigens, CD19Antigens, Differentiation, B-LymphocyteCross-Linking ReagentsFc gamma receptor IIBInterleukin-21InterleukinsReceptors, Antigen, B-CellReceptors, IgGToll-Like Receptors

Identifiers

PMID24442430
PMCPMC3918864
OpenAlexW2167272043

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.