Evidence map›Paper›PMID 21235532›Full record

ArticleClinical and experimental immunology2011

B cell-targeted therapy with anti-CD20 monoclonal antibody in a mouse model of Graves' hyperthyroidism.

I Ueki, N Abiru, M Kobayashi, M Nakahara, T Ichikawa, K Eguchi, Y Nagayama

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2011. 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
2.3field-weighted citation impact, top 12% 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, 28 citations in OpenAlex.

  1. Article
  2. Marginal zone B cells are required for optimal humoral responses to allograft.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Rejection of xenogeneic porcine islets in humanized mice is characterized by graft-infiltrating Th17 cells and activated B cells.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2020
    Article
  7. Review
  8. Article
  9. Article
  10. An update on the medical treatment of Graves' hyperthyroidism.Journal of endocrinological investigation · 2014
    Review
  11. Review
  12. Article
  13. Article
  14. Blocking type TSH receptor antibodies.Auto- immunity highlights · 2013
    Review
  15. 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 2 institutions in 1 country.

I UekiDepartment of Medical Gene Technology, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
N Abiru
M Kobayashi
M Nakahara
T Ichikawa
K Eguchi
Y Nagayama
Hiroshima Red Cross Hospital & Atomic-bomb Survivors Hospital · JPNagasaki University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Graves' disease is a B cell-mediated and T cell-dependent autoimmune disease of the thyroid which is characterized by overproduction of thyroid hormones and thyroid enlargement by agonistic anti-thyrotrophin receptor (TSHR) autoantibody. In addition to antibody secretion, B cells have recently been recognized to function as antigen-presenting/immune-modulatory cells. The present study was designed to evaluate the efficacy of B cell depletion by anti-mouse (m) CD20 monoclonal antibody (mAb) on Graves' hyperthyroidism in a mouse model involving repeated injection of adenovirus expressing TSHR A-subunit (Ad-TSHR289). We observe that a single injection of 250 µg/mouse anti-mCD20 mAb eliminated B cells efficiently from the periphery and spleen and to a lesser extent from the peritoneum for more than 3 weeks. B cell depletion before immunization suppressed an increase in serum immunoglobulin (Ig)G levels, TSHR-specific splenocyte secretion of interferon (IFN)-γ, anti-TSHR antibody production and development of hyperthyroidism. B cell depletion 2 weeks after the first immunization, a time-point at which T cells were primed but antibody production was not observed, was still effective at inhibiting antibody production and disease development without inhibiting splenocyte secretion of IFN-γ. By contrast, B cell depletion in hyperthyroid mice was therapeutically ineffective. Together, these data demonstrate that B cells are critical not only as antibody-producing cells but also as antigen-presenting/immune-modulatory cells in the early phase of the induction of experimental Graves' hyperthyroidism and, although therapeutically less effective, B cell depletion is highly efficient for preventing disease development.

Indexed as

AnimalsAntibodies, MonoclonalAntigens, CD20B-LymphocytesCell CountDisease Models, AnimalFemaleGraves DiseaseImmunoglobulin GImmunoglobulins, Thyroid-StimulatingInterferon-gammaLymphocyte ActivationLymphocyte CountLymphocyte DepletionMiceMice, Inbred BALB CAntibodies, MonoclonalAntigens, CD20Immunoglobulin GImmunoglobulins, Thyroid-StimulatingInterferon-gammaReceptors, ThyrotropinThyroxineVaccines, DNA

Identifiers

PMID21235532
PMCPMC3048613
OpenAlexW1538688491

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.