Evidence map›Paper›PMID 25505278›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

CCR2-dependent dendritic cell accumulation in the central nervous system during early effector experimental autoimmune encephalomyelitis is essential for effector T cell restimulation in situ and disease progression.

Benjamin D Clarkson, Alec Walker, Melissa G Harris, Aditya Rayasam, Matyas Sandor, Zsuzsanna Fabry

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.0field-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

47 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Paradoxical Expression of Ionotropic Glutamate Receptors in Leucocytes.Clinical reviews in allergy & immunology · 2026
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  5. An IL-23-STAT4 pathway is required for the proinflammatory function of classical dendritic cells during CNS inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  6. Review
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  11. Review
  12. Upregulation of Inflammatory Mediators in Peripheral Blood CD40International journal of molecular sciences · 2023
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Molecular Mechanisms of Neuroimmune Crosstalk in the Pathogenesis of Stroke.International journal of molecular sciences · 2021
    Review
  20. 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

6 authors at 2 institutions in 1 country.

Benjamin D ClarksonDepartment of Pathology, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI 53792; Department of Laboratory Medicine, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI 53792; Graduate Training Program of Cellular and Molecular Pathology, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI 53792; and.
Alec WalkerDepartment of Pathology, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI 53792; Department of Laboratory Medicine, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI 53792;
Melissa G HarrisDepartment of Pathology, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI 53792; Department of Laboratory Medicine, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI 53792;
Aditya RayasamGraduate Training Program of Neuroscience, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI 53792.
Matyas SandorDepartment of Pathology, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI 53792; Department of Laboratory Medicine, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI 53792;
Zsuzsanna FabryDepartment of Pathology, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI 53792; Department of Laboratory Medicine, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI 53792; zfabry@wisc.edu.
University of Wisconsin–Madison · USWisconsin Division of Public Health · US

Funding

NEUROSCIENCE TRAINING PROGRAMT32GM007507 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI HALLORAN, MARY C · 1985 to 2017
$9.3M
ANTIGEN SPECIFIC T CELL ACCUMULATION IN THE CNSR01NS037570 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI FABRY, ZSUZSANNA · 2000 to 2012
$3.1M
Graduate Training In Cellular And Molecular Pathogenesis Of Human DiseasesT32GM081061 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI FABRY, ZSUZSANNA · 2010 to 2019
$1.8M
CNS TuberculosisR01NS076946 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI FABRY, ZSUZSANNA · 2012 to 2016
$1.7M
Antigen specific T cell accumulation in the CNSR56NS037570 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI FABRY, ZSUZSANNA · 2008 to 2008
$367k
NIGMS NIH HHS T32 GM007507NIGMS NIH HHS T32GM081061NINDS NIH HHS NS076946-01A1NINDS NIH HHS NS37570-01A2NINDS NIH HHS R01 NS037570NINDS NIH HHS R01 NS076946NINDS NIH HHS R56 NS037570
6 · The paper itself

Abstract

Dendritic cells (DCs)--although absent from the healthy CNS parenchyma--rapidly accumulate within brain and spinal cord tissue during neuroinflammation associated with experimental autoimmune encephalomyelitis (EAE; a mouse model of multiple sclerosis). Yet, although DCs have been appreciated for their role in initiating adaptive immune responses in peripheral lymphoid organ tissues, how DCs infiltrate the CNS and contribute to ongoing neuroinflammation in situ is poorly understood. In this study, we report the following: 1) CD11c(+) bone marrow-derived DCs and CNS-infiltrating DCs express chemokine receptor CCR2; 2) compared with CCR2(+/+) cells, adoptively transferred CCR2(-/-) bone marrow-derived DCs or DC precursors do not accumulate in the CNS during EAE, despite abundance in blood; 3) CCR2(-/-) DCs show less accumulation in the inflamed CNS in mixed bone marrow chimeras, when compared with CCR2(+/+) DCs; and 4) ablation of CCR2(+/+) DCs during EAE clinical onset delays progression and attenuates cytokine production by infiltrating T cells. Whereas the role of CCR2 in monocyte migration into the CNS has been implicated previously, the role of CCR2 in DC infiltration into the CNS has never been directly addressed. Our data suggest that CCR2-dependent DC recruitment to the CNS during ongoing neuroinflammation plays a crucial role in effector T cell cytokine production and disease progression, and signify that CNS-DCs and circulating DC precursors might be key therapeutic targets for suppressing ongoing neuroinflammation in CNS autoimmune diseases.

Indexed as

Adoptive TransferAnimalsBone Marrow CellsBone Marrow TransplantationBrainCell MovementCytokinesDendritic CellsEncephalomyelitis, Autoimmune, ExperimentalInflammationMiceMice, KnockoutMonocytesReceptors, CCR2Spinal CordT-LymphocytesCcr2 protein, mouseCytokinesReceptors, CCR2

Identifiers

PMID25505278
PMCPMC4362728
OpenAlexW1885124648

What OpenQuestion holds

Textmetadata
LicenceTDM
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.