Evidence map›Paper›PMID 25101629›Full record

ArticlePloS one2014

Germinal center B cell depletion diminishes CD4+ follicular T helper cells in autoimmune mice.

Isharat Yusuf, Jessica Stern, Tom M McCaughtry, Sandra Gallagher, Hong Sun, Changshou Gao, Thomas Tedder, Gianluca Carlesso, Laura Carter, Ronald Herbst and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Modeling the Synergetic Dynamics of B cells and TbioRxiv : the preprint server for biology · 2025
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  3. T-Cell/B-Cell Interactions in Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2024
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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

11 authors at 1 institution in 1 country.

Isharat YusufDepartment of Respiratory, Inflammation and Autoimmunity Research, MedImmune LLC, Gaithersburg, Maryland, United States of America.
Jessica SternDepartment of Respiratory, Inflammation and Autoimmunity Research, MedImmune LLC, Gaithersburg, Maryland, United States of America.
Tom M McCaughtryDepartment of Respiratory, Inflammation and Autoimmunity Research, MedImmune LLC, Gaithersburg, Maryland, United States of America.
Sandra GallagherDepartment of Respiratory, Inflammation and Autoimmunity Research, MedImmune LLC, Gaithersburg, Maryland, United States of America.
Hong SunDepartment of Respiratory, Inflammation and Autoimmunity Research, MedImmune LLC, Gaithersburg, Maryland, United States of America.
Changshou GaoDepartment of Antibody Discovery and Protein Engineering, MedImmune LLC, Gaithersburg, Maryland, United States of America.
Thomas TedderDepartment of Immunology, Duke University Medical Center, Durham, North Carolina, United States of America.
Gianluca CarlessoDepartment of Respiratory, Inflammation and Autoimmunity Research, MedImmune LLC, Gaithersburg, Maryland, United States of America.
Laura CarterDepartment of Respiratory, Inflammation and Autoimmunity Research, MedImmune LLC, Gaithersburg, Maryland, United States of America.
Ronald HerbstDepartment of Respiratory, Inflammation and Autoimmunity Research, MedImmune LLC, Gaithersburg, Maryland, United States of America.
Yue WangDepartment of Respiratory, Inflammation and Autoimmunity Research, MedImmune LLC, Gaithersburg, Maryland, United States of America.
Duke Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundContinuous support from follicular CD4(+) T helper (Tfh) cells drives germinal center (GC) responses, which last for several weeks to produce high affinity memory B cells and plasma cells. In autoimmune Sle1 and NZB/W F1 mice, elevated numbers of Tfh cells persist, promoting the expansion of self-reactive B cells. Expansion of circulating Tfh like cells have also been described in several autoimmune diseases. Although, the signals required for Tfh differentiation have now been well described, the mechanisms that sustain the maintenance of fully differentiated Tfh are less understood. Recent data demonstrate a role for GC B cells for Tfh maintenance after protein immunization. METHODS AND FINDING: Given the pathogenic role Tfh play in autoimmune disease, we explored whether B cells are required for maintenance of autoreactive Tfh. Our data suggest that the number of mature autoreactive Tfh cells is controlled by GC B cells. Depletion of B cells in Sle1 autoimmune mice leads to a dramatic reduction in Tfh cells. In NZB/W F1 autoimmune mice, similar to the SRBC immunization model, GC B cells support the maintenance of mature Tfh, which is dependent mainly on ICOS. The CD28-associated pathway is dispensable for Tfh maintenance in SRBC immunized mice, but is required in the spontaneous NZB/W F1 model.

conclusionThese data suggest that mature Tfh cells require signals from GC B cells to sustain their optimal numbers and function in both autoimmune and immunization models. Thus, immunotherapies targeting B cells in autoimmune disease may affect pathogenic Tfh cells.

Indexed as

Models, ImmunologicalAnimalsAutoimmune DiseasesB-LymphocytesCell DifferentiationGerminal CenterMice, Inbred BALB CMice, Inbred C57BLMice, Inbred NZBSignal TransductionT-Lymphocytes, Helper-Inducer

Identifiers

PMID25101629
PMCPMC4125140
OpenAlexW2038041677

What OpenQuestion holds

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LicenceCC BY
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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.