Evidence map›Paper›PMID 25010693›Full record

ArticlePloS one2014

Neutrophils contribute to excess serum BAFF levels and promote CD4+ T cell and B cell responses in lupus-prone mice.

Christine M Coquery, Nekeithia S Wade, William M Loo, Jason M Kinchen, Kelly M Cox, Chao Jiang, Kenneth S Tung, Loren D Erickson

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 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Christine M CoqueryDepartment of Microbiology, Immunology, and Cancer Biology, University of Virginia, Charlottesville, Virginia, United States of America; Beirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, Virginia, United States of America.
Nekeithia S WadeBeirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, Virginia, United States of America.
William M LooBeirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, Virginia, United States of America.
Jason M KinchenDepartment of Microbiology, Immunology, and Cancer Biology, University of Virginia, Charlottesville, Virginia, United States of America; Beirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, Virginia, United States of America; Center for Cell Clearance, University of Virginia, Charlottesville, Virginia, United States of America.
Kelly M CoxDepartment of Microbiology, Immunology, and Cancer Biology, University of Virginia, Charlottesville, Virginia, United States of America; Beirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, Virginia, United States of America.
Chao JiangDivision of Extramural Research, National Institutes of Health, Bethesda, Maryland, United States of America.
Kenneth S TungBeirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, Virginia, United States of America; Department of Pathology, University of Virginia, Charlottesville, Virginia, United States of America.
Loren D EricksonDepartment of Microbiology, Immunology, and Cancer Biology, University of Virginia, Charlottesville, Virginia, United States of America; Beirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, Virginia, United States of America.
Carter Center · USOffice of Extramural Research · USUniversity of Virginia · US

Funding

Women's Oncology Program - WONP30CA044579 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Thomas P. Loughran · 1987 to 2026
$72.1M
INTERDISCIPLINARY TRAINING PROGRAM IN IMMUNOLOGYT32AI007496 · NIAID · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Michael G. Brown, Coleen A McNamara · 1995 to 2026
$10.2M
Testosterone-GnRH Frequency and the Evolution of PCOS in AdolescenceP50HD028934 · NICHD · UNIVERSITY OF VIRGINIA · PI HAISENLEDER, DANIEL J. · 2014 to 2018
$8.6M
ZONA PELLUCIDA--IMMUNOPATHOLOGIC STUDYR01AI041236 · NIAID · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI TUNG, KENNETH S.K. · 1996 to 2017
$5.2M
Pathways of plasma cell differentiation in autoimmunityR01AI093722 · NIAID · UNIVERSITY OF VIRGINIA · PI ERICKSON, LOREN D · 2012 to 2016
$2.0M
The Role of B Cell Maturation Antigen in Controlling ToleranceF31AR064145 · NIAMS · UNIVERSITY OF VIRGINIA · PI COQUERY, CHRISTINE MOREL · 2013 to 2014
$34k
NCI NIH HHS P30 CA044579NIAID NIH HHS R01 AI041236NIAID NIH HHS R01 AI 093722NIAID NIH HHS R01 AI093722NIAID NIH HHS T32 AI007496NIAMS NIH HHS F31 AR 064145NIAMS NIH HHS F31 AR064145NICHD NIH HHS P50 HD028934PHS HHS 5T32A1007496-19
6 · The paper itself

Abstract

Despite increased frequencies of neutrophils found in autoimmune diseases such as systemic lupus erythematosus (SLE), how they contribute to disease pathogenesis and the mechanisms that affect the accumulation of neutrophils are poorly understood. The aim of this study was to identify factors in autoantibody-mediated autoimmunity that controls the accumulation of spleen resident neutrophils and to determine whether neutrophils contribute to abnormal B cell responses. Increased levels of the cytokine BAFF have been linked to loss of B cell tolerance in autoimmunity, but the cellular source responsible for excess BAFF is unknown. B cell maturation antigen (BCMA) is a receptor for BAFF and is critical for the survival of bone marrow plasma cells. Paradoxically, BCMA deficiency exacerbates the formation of autoantibody-secreting plasma cells in spleens of lupus-prone mice and the reasons for this effect are not understood. Here we analyzed the phenotype, localization and function of neutrophils in spleens of healthy mice and congenic lupus-prone mice, and compared mice sufficient or deficient in BCMA expression. Neutrophils were found to be significantly increased in frequency and activation status in spleens of lupus-prone mice when BCMA was absent. Furthermore, neutrophils localized within T cell zones and enhanced CD4(+) T cell proliferation and IFNγ production through the production of BAFF. Reduced BAFF and IFNγ serum levels, decreased frequencies of IFNγ-producing T cells, germinal center B cells, and autoantibody production after neutrophil depletion indicated the involvement of neutrophils in these autoimmune traits. Thus, we have identified a novel role for BCMA to control excess BAFF production in murine lupus through restraining the accumulation of BAFF-producing neutrophils. Our data suggests that devising therapeutic strategies to reduce neutrophils in autoimmunity may decrease BAFF levels and ameliorate disease.

Indexed as

AnimalsAutoimmunityB-Cell Activating FactorB-Cell Maturation AntigenB-LymphocytesCD4-Positive T-LymphocytesDisease Models, AnimalFemaleHumansLupus Erythematosus, SystemicMiceNeutrophilsSpleenT-LymphocytesB-Cell Activating FactorB-Cell Maturation AntigenTnfsf13b protein, mouse

Identifiers

PMID25010693
PMCPMC4092127
OpenAlexW2011340425

What OpenQuestion holds

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LicenceCC0
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.