Evidence map›Paper›PMID 28039405›Full record

ArticlePhysiological reports2016

Role of BAFF in pulmonary autoantibody responses induced by chronic cigarette smoke exposure in mice.

Mathieu C Morissette, Yang Gao, Pamela Shen, Danya Thayaparan, Jean-Christophe Bérubé, Peter D Paré, Corry-Anke Brandsma, Ke Hao, Yohan Bossé, Rachel Ettinger and 6 more

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-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

22 citing papers in PubMed, 27 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

16 authors at 8 institutions in 4 countries.

Mathieu C MorissetteDepartment of Pathology and Molecular Medicine, McMaster Immunology Research Centre, McMaster University, Hamilton, Ontario, Canada.
Yang GaoDepartment of Pathology and Molecular Medicine, McMaster Immunology Research Centre, McMaster University, Hamilton, Ontario, Canada.
Pamela ShenMedical Sciences Graduate Program, McMaster University, Hamilton, Ontario, Canada.
Danya ThayaparanMedical Sciences Graduate Program, McMaster University, Hamilton, Ontario, Canada.
Jean-Christophe BérubéCentre de Recherche de l'Institut universitaire de cardiologie et de pneumologie de Québec, Québec, Canada.
Peter D ParéDepartment of Medicine & Center for Heart Lung Innovation, University of British Columbia St. Paul's Hospital, Vancouver, Canada.
Corry-Anke BrandsmaGroningen Research Institute for Asthma and COPD (GRIAC), University of Groningen University Medical Center Groningen, Groningen, The Netherlands.
Ke HaoDepartment of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York City, New York.
Yohan BosséCentre de Recherche de l'Institut universitaire de cardiologie et de pneumologie de Québec, Québec, Canada.
Rachel EttingerMedImmune LLC, Gaithersburg, Maryland.
Ronald HerbstMedImmune LLC, Gaithersburg, Maryland.
Alison A HumblesMedImmune LLC, Gaithersburg, Maryland.
Roland KolbeckMedImmune LLC, Gaithersburg, Maryland.
Nanshan ZhongState Key Laboratory of Respiratory Disease, and Guangzhou Institute of Respiratory Disease, First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Rongchang ChenState Key Laboratory of Respiratory Disease, and Guangzhou Institute of Respiratory Disease, First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Martin R StämpfliDepartment of Pathology and Molecular Medicine, McMaster Immunology Research Centre, McMaster University, Hamilton, Ontario, Canada stampfli@mcmaster.ca.
Institut universitaire de cardiologie et de pneumologie de Québec · CAMcMaster University · CAMcMaster University Medical Centre · CAState Key Laboratory of Respiratory Disease · CNFirst Affiliated Hospital of Guangzhou Medical University · CNIcahn School of Medicine at Mount Sinai · USUniversity of British Columbia · CAUniversity of Groningen · NL

Funding

Canadian Institutes of Health Research CCI‐132573Canadian Institutes of Health Research MOP# 64390
6 · The paper itself

Abstract

Emerging evidence suggests that autoimmune processes are implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). In this study, we assessed the expression of B-cell activating factor (BAFF) in smokers, and investigated the functional importance of BAFF in the induction and maintenance of cigarette smoke-induced pulmonary antinuclear antibodies (ANA) and tertiary lymphoid tissues (TLTs) using a preclinical mouse model. We observed that BAFF levels were elevated in smokers and mice exposed to cigarette smoke. In mice, BAFF expression was rapidly induced in the lungs following 4 days of cigarette smoke exposure and remained elevated following 8 and 24 weeks of exposure. Alveolar macrophages were the major source of BAFF Blockade of BAFF using a BAFF receptor-Fc (BAFFR-Fc) construct prevented pulmonary ANA and TLT formation when delivered concurrent with cigarette smoke exposure. Under these conditions, no impact on lung inflammation was observed. However, administration of BAFFR-Fc following smoking cessation markedly reduced the number of TLTs and ANA levels and, of note, reduced pulmonary neutrophilia. Altogether, this study shows for the first time a central role of BAFF in the induction and maintenance of cigarette smoke-induced pulmonary ANA and suggests that BAFF blockade following smoking cessation could have beneficial effects on persistent inflammatory processes.In this study, we assessed the expression of B-cell activating factor (BAFF) in smokers, and investigated the functional importance of BAFF in the induction and maintenance of cigarette smoke-induced pulmonary antinuclear antibodies (ANA) and tertiary lymphoid tissues (TLTs) using a preclinical mouse model. Data presented show that BAFF plays a central role in the induction and maintenance of cigarette smoke-induced pulmonary ANA and suggest a therapeutic potential for BAFF blockade in limiting autoimmune processes associated with smoking.

Indexed as

AnimalsAntibodies, AntinuclearB-Cell Activating FactorB-LymphocytesCigarette SmokingFemaleHumansImmunoglobulin MLungMaleMiceMice, Inbred BALB CMiddle AgedNicotianaSmoking CessationSpleenAntibodies, AntinuclearB-Cell Activating FactorImmunoglobulin MTNFSF13B protein, humanTnfsf13b protein, mouseAnimal modelautoantibodiesBAFFcigarette smokeCOPD

Identifiers

PMID28039405
PMCPMC5210376
OpenAlexW2562252494

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.