Evidence map›Paper›PMID 15210744›Full record

ArticleThe Journal of experimental medicine2004

The innate mononuclear phagocyte network depletes B lymphocytes through Fc receptor-dependent mechanisms during anti-CD20 antibody immunotherapy.

Junji Uchida, Yasuhito Hamaguchi, Julie A Oliver, Jeffrey V Ravetch, Jonathan C Poe, Karen M Haas, Thomas F Tedder

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 272 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
272citing papers in PubMed, 1 pooled it
28.8field-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

272 citing papers in PubMed, 1 synthesis or guideline pooled it, 629 citations in OpenAlex.

  1. Pooled it
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  7. Low Serum Vitamin D Levels Are Associated With Inferior Survival in Follicular Lymphoma: A Prospective Evaluation in SWOG and LYSA Studies.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2015
    Trial
  8. Trial
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  11. Fc-engineering for improved cancer immunotherapy.Biochemical Society transactions · 2026
    Review
  12. Article
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  14. Tailored FcγR blockade enhances immune checkpoint therapy and overcomes resistance.Journal of experimental & clinical cancer research : CR · 2026
    Article
  15. Article
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  17. Review
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  20. Article

212 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

7 authors at 3 institutions in 1 country.

Junji UchidaDepartment of Immunology, Box 3010, Room 353 Jones Building, Research Drive, Duke University Medical Center, Durham, NC 27710, USA.
Yasuhito Hamaguchi
Julie A Oliver
Jeffrey V Ravetch
Jonathan C Poe
Karen M Haas
Thomas F Tedder
Duke Medical Center · USDuke University Hospital · 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
NCI NIH HHS CA96547NCI NIH HHS R01 CA096547NIAID NIH HHS AI56363NIAID NIH HHS U19 AI056363
6 · The paper itself

Abstract

Anti-CD20 antibody immunotherapy effectively treats non-Hodgkin's lymphoma and autoimmune disease. However, the cellular and molecular pathways for B cell depletion remain undefined because human mechanistic studies are limited. Proposed mechanisms include antibody-, effector cell-, and complement-dependent cytotoxicity, the disruption of CD20 signaling pathways, and the induction of apoptosis. To identify the mechanisms for B cell depletion in vivo, a new mouse model for anti-CD20 immunotherapy was developed using a panel of twelve mouse anti-mouse CD20 monoclonal antibodies representing all four immunoglobulin G isotypes. Anti-CD20 antibodies rapidly depleted the vast majority of circulating and tissue B cells in an isotype-restricted manner that was completely dependent on effector cell Fc receptor expression. B cell depletion used both FcgammaRI- and FcgammaRIII-dependent pathways, whereas B cells were not eliminated in FcR common gamma chain-deficient mice. Monocytes were the dominant effector cells for B cell depletion, with no demonstrable role for T or natural killer cells. Although most anti-CD20 antibodies activated complement in vitro, B cell depletion was completely effective in mice with genetic deficiencies in C3, C4, or C1q complement components. That the innate monocyte network depletes B cells through FcgammaR-dependent pathways during anti-CD20 immunotherapy has important clinical implications for anti-CD20 and other antibody-based therapies.

Indexed as

AnimalsAntigens, CD20B-LymphocytesImmunotherapyLeukocytes, MononuclearLymphocyte DepletionMiceMice, KnockoutPhagocytesReceptors, IgGSpleenAntigens, CD20Fcgr3 protein, mouseReceptors, IgG

Identifiers

PMID15210744
PMCPMC2212805
OpenAlexW2108556253

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.