Evidence map›Paper›PMID 16520392›Full record

ArticleThe Journal of experimental medicine2006

Antibody isotype-specific engagement of Fcgamma receptors regulates B lymphocyte depletion during CD20 immunotherapy.

Yasuhito Hamaguchi, Yan Xiu, Kazuhiro Komura, Falk Nimmerjahn, Thomas F Tedder

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
18.3field-weighted citation impact, top 1% 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

85 citing papers in PubMed, 234 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. FcFrontiers in immunology · 2022
    Article
  18. Review
  19. Article
  20. Article

25 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Yasuhito HamaguchiDepartment of Immunology, Duke University Medical Center, Durham, NC 27710, USA.
Yan Xiu
Kazuhiro Komura
Falk Nimmerjahn
Thomas F Tedder
Duke Medical Center · USRockefeller University · US

Funding

Supplement - Inflammatory Triggers in B Cell AutoimmunityU19AI056363 · NIAID · DUKE UNIVERSITY · PI ST. CLAIR, EUGENE WILLIAM · 2003 to 2017
$35.3M
CD22 Regulation of B Lymphocyte Function and SurvivalR01CA096547 · NCI · DUKE UNIVERSITY · PI TEDDER, THOMAS F · 2003 to 2007
$1.3M
MS4A Family Members in Health and DiseaseR01CA105001 · NCI · DUKE UNIVERSITY · PI TEDDER, THOMAS F · 2004 to 2008
$1.2M
NCI NIH HHS CA105001NCI NIH HHS CA96547NCI NIH HHS R01 CA096547NCI NIH HHS R01 CA105001NIAID NIH HHS AI56363NIAID NIH HHS U19 AI056363
6 · The paper itself

Abstract

CD20 monoclonal antibody (mAb) immunotherapy is effective for lymphoma and autoimmune disease. In a mouse model of immunotherapy using mouse anti-mouse CD20 mAbs, the innate monocyte network depletes B cells through immunoglobulin (Ig)G Fc receptor (FcgammaR)-dependent pathways with a hierarchy of IgG2a/c>IgG1/IgG2b>IgG3. To understand the molecular basis for these CD20 mAb subclass differences, B cell depletion was assessed in mice deficient or blocked for stimulatory FcgammaRI, FcgammaRIII, FcgammaRIV, or FcR common gamma chain, or inhibitory FcgammaRIIB. IgG1 CD20 mAbs induced B cell depletion through preferential, if not exclusive, interactions with low-affinity FcgammaRIII. IgG2b CD20 mAbs interacted preferentially with intermediate affinity FcgammaRIV. The potency of IgG2a/c CD20 mAbs resulted from FcgammaRIV interactions, with potential contributions from high-affinity FcgammaRI. Regardless, FcgammaRIV could mediate IgG2a/b/c CD20 mAb-induced depletion in the absence of FcgammaRI and FcgammaRIII. In contrast, inhibitory FcgammaRIIB deficiency significantly increased CD20 mAb-induced B cell depletion by enhancing monocyte function. Although FcgammaR-dependent pathways regulated B cell depletion from lymphoid tissues, both FcgammaR-dependent and -independent pathways contributed to mature bone marrow and circulating B cell clearance by CD20 mAbs. Thus, isotype-specific mAb interactions with distinct FcgammaRs contribute significantly to the effectiveness of CD20 mAbs in vivo, which may have important clinical implications for CD20 and other mAb-based therapies.

Indexed as

Lymphocyte DepletionAnimalsAntibodies, MonoclonalAntigens, CD20Autoimmune DiseasesB-LymphocytesDose-Response Relationship, DrugDose-Response Relationship, ImmunologicDrug Evaluation, PreclinicalImmunoglobulin GLymphomaMiceMonocytesReceptors, IgGAntibodies, MonoclonalAntigens, CD20Immunoglobulin GReceptors, IgG

Identifiers

PMID16520392
PMCPMC2118227
OpenAlexW2048787440

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.