Evidence map›Paper›PMID 34479995›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2021

Bcl6 controls meningeal Th17-B cell interaction in murine neuroinflammation.

Maike Hartlehnert, Anna-Lena Börsch, Xiaolin Li, Miriam Burmeister, Hanna Gerwien, David Schafflick, Michael Heming, I-Na Lu, Venu Narayanan, Jan-Kolja Strecker and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  3. ODC1 restricts meningeal B cell age-associated-like phenotype and function in multiple sclerosis: A human and experimental study.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  12. Myelin-reactive B cells exacerbate CD4Nature communications · 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

16 authors at 4 institutions in 2 countries.

Maike HartlehnertDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, Germany.
Anna-Lena BörschDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, Germany.ORCID 0000-0001-9174-8652
Xiaolin LiDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, Germany.ORCID 0000-0003-1524-051X
Miriam BurmeisterInstitute of Physiological Chemistry and Pathobiochemistry, University of Münster, 48149 Münster, Germany.ORCID 0000-0001-7716-5901
Hanna GerwienInstitute of Physiological Chemistry and Pathobiochemistry, University of Münster, 48149 Münster, Germany.ORCID 0000-0001-8372-7288
David SchafflickDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, Germany.ORCID 0000-0001-5908-4745
Michael HemingDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, Germany.ORCID 0000-0002-9568-2790
I-Na LuDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, Germany.
Venu NarayananDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, Germany.
Jan-Kolja StreckerDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, Germany.
Anna KolzInstitute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians University Munich, 81377 Munich, Germany.ORCID 0000-0002-6020-7746
Anneli PetersInstitute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians University Munich, 81377 Munich, Germany.
Gregory F WuDepartment of Neurology, Washington University in St. Louis, St. Louis, MO 63108.ORCID 0000-0003-3588-0637
Heinz WiendlDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, Germany.
Lydia SorokinInstitute of Physiological Chemistry and Pathobiochemistry, University of Münster, 48149 Münster, Germany.ORCID 0000-0001-7704-7921
Gerd Meyer Zu HorsteDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, Germany; gerd.meyerzuhoerste@ukmuenster.de.ORCID 0000-0002-4341-4719
University Hospital Münster · DEUniversity of Münster · DELudwig-Maximilians-Universität München · DEWashington University in St. Louis · US

Funding

The Role of TRPV4 in central nervous system immunity and diseaseR01NS106289 · NINDS · WASHINGTON UNIVERSITY · PI WU, GREGORY · 2018 to 2021
$1.6M
NINDS NIH HHS R01 NS106289
6 · The paper itself

Abstract

Ectopic lymphoid tissue containing B cells forms in the meninges at late stages of human multiple sclerosis (MS) and when neuroinflammation is induced by interleukin (IL)-17 producing T helper (Th17) cells in rodents. B cell differentiation and the subsequent release of class-switched immunoglobulins have been speculated to occur in the meninges, but the exact cellular composition and underlying mechanisms of meningeal-dominated inflammation remain unknown. Here, we performed in-depth characterization of meningeal versus parenchymal Th17-induced rodent neuroinflammation. The most pronounced cellular and transcriptional differences between these compartments was the localization of B cells exhibiting a follicular phenotype exclusively to the meninges. Correspondingly, meningeal but not parenchymal Th17 cells acquired a B cell-supporting phenotype and resided in close contact with B cells. This preferential B cell tropism for the meninges and the formation of meningeal ectopic lymphoid tissue was partially dependent on the expression of the transcription factor Bcl6 in Th17 cells that is required in other T cell lineages to induce isotype class switching in B cells. A function of Bcl6 in Th17 cells was only detected in vivo and was reflected by the induction of B cell-supporting cytokines, the appearance of follicular B cells in the meninges, and of immunoglobulin class switching in the cerebrospinal fluid. We thus identify the induction of a B cell-supporting meningeal microenvironment by Bcl6 in Th17 cells as a mechanism controlling compartment specificity in neuroinflammation.

Indexed as

AnimalsB-LymphocytesCell CommunicationCytokinesEncephalomyelitis, Autoimmune, ExperimentalFemaleGerminal CenterInflammationLymphocyte ActivationMaleMeningesMiceMice, Inbred C57BLMultiple SclerosisNeuroinflammatory DiseasesParenchymal TissueBcl6 protein, mouseCytokinesProto-Oncogene Proteins c-bcl-6Bcl6CNS meningesectopic lymphoid tissuesingle-cell RNA-seqTh17

Identifiers

PMID34479995
PMCPMC8433502
OpenAlexW3196356589

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.