Evidence map›Paper›PMID 20368280›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

Protective and pathogenic roles for B cells during systemic autoimmunity in NZB/W F1 mice.

Karen M Haas, Rei Watanabe, Takashi Matsushita, Hiroko Nakashima, Nobuko Ishiura, Hitoshi Okochi, Manabu Fujimoto, Thomas F Tedder

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

82 citing papers in PubMed, 148 citations in OpenAlex.

  1. Article
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  6. AFrontiers in tuberculosis · 2026
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22 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

8 authors at 3 institutions in 2 countries.

Karen M HaasDepartment of Immunology, Duke University Medical Center, Durham, NC 27710, USA.
Rei Watanabe
Takashi Matsushita
Hiroko Nakashima
Nobuko Ishiura
Hitoshi Okochi
Manabu Fujimoto
Thomas F Tedder
Saitama International Medical Center · JPDuke Medical Center · USKanazawa University · JP

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

Delineating the relative contributions of B lymphocytes during the course of autoimmune disease has been difficult. Therefore, the effects of depleting all mature B cells using a potent CD20 mAb, or of depleting circulating and marginal zone B cells using a ligand-blocking CD22 mAb, were compared in NZB/W F(1) mice, a model for human systemic lupus erythematosus. Single low-dose mAb treatments depleted B cells efficiently in both NZB/W F(1) and C57BL/6 mice. Prophylactic B cell depletion by repeated CD20 mAb treatments prolonged survival during pristane-accelerated lupus in NZB/W F(1) mice, whereas CD22 mAb had little effect. Despite effective B cell depletion, neither mAb treatment prevented autoantibody generation. In addition, CD20, CD22, and control mAb-treated NZB/W F(1) mice developed anti-mouse IgG autoantibodies in contrast to parental NZB and NZW strains, which may have reduced the effectiveness of B cell depletion. Despite this, low-dose CD20 mAb treatment initiated in 12-28-wk-old mice, and administered every 4 wk thereafter, significantly delayed spontaneous disease in NZB/W F(1) mice. By contrast, B cell depletion initiated in 4-wk-old mice hastened disease onset, which paralleled depletion of the IL-10-producing regulatory B cell subset called B10 cells. B10 cells were phenotypically similar in NZB/W F(1) and C57BL/6 mice, but were expanded significantly in young NZB/W F(1) mice. Thus, B cell depletion had significant effects on NZB/W F(1) mouse survival that were dependent on the timing of treatment initiation. Therefore, distinct B cell populations can have opposing protective and pathogenic roles during lupus progression.

Indexed as

AnimalsAntibodies, MonoclonalAntigens, CD20AutoantibodiesB-Lymphocyte SubsetsCrosses, GeneticDisease Models, AnimalFemaleLupus Erythematosus, SystemicLupus NephritisLymphocyte CountLymphocyte DepletionMaleMiceMice, Inbred C57BLMice, Inbred NZBAntibodies, MonoclonalAntigens, CD20AutoantibodiesCd22 protein, mousepristaneSialic Acid Binding Ig-like Lectin 2Terpenes

Identifiers

PMID20368280
PMCPMC3734557
OpenAlexW1895521524

What OpenQuestion holds

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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.