Evidence map›Paper›PMID 24924222›Full record

ArticleJournal of neuroinflammation2014

Deletion of astroglial CXCL10 delays clinical onset but does not affect progressive axon loss in a murine autoimmune multiple sclerosis model.

Emily Mills Ko, Joyce H Ma, Fuzheng Guo, Laird Miers, Eunyoung Lee, Peter Bannerman, Travis Burns, David Ko, Jiho Sohn, Athena M Soulika and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

56 citing papers in PubMed, 100 citations in OpenAlex.

  1. Glial cells in neuropathic pain.Physiological reviews · 2026
    Review
  2. Astrocytes in Multiple Sclerosis: Getting to the Core.International journal of molecular sciences · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
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  11. T Cells Trafficking into the Brain in Aging and Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
    Review
  12. Article
  13. Review
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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 2 institutions in 2 countries.

Emily Mills Ko
Joyce H Ma
Fuzheng Guo
Laird Miers
Eunyoung Lee
Peter Bannerman
Travis Burns
David Ko
Jiho Sohn
Athena M SoulikaInstitute for Pediatric Regenerative Medicine, UC Davis School of Medicine and Shriners Hospital, 2425 Stockton Blvd, Sacramento, CA 95817, USA. athena.soulika@ucdmc.ucdavis.edu.
David Pleasure
University of California, Davis · USShriners Hospitals for Children - Erie · US

Funding

OLIGODENDROGLIAL PROLIFERATION AND DIFFERENTIATIONR01NS025044 · NINDS · UNIVERSITY OF CALIFORNIA DAVIS · PI PLEASURE, DAVID E. · 1987 to 2011
$3.9M
NINDS NIH HHS R01 NS025044
6 · The paper itself

Abstract

Multiple sclerosis (MS) is characterized by central nervous system (CNS) inflammation, demyelination, and axonal degeneration. CXCL10 (IP-10), a chemokine for CXCR3+ T cells, is known to regulate T cell differentiation and migration in the periphery, but effects of CXCL10 produced endogenously in the CNS on immune cell trafficking are unknown. We created floxed cxcl10 mice and crossed them with mice carrying an astrocyte-specific Cre transgene (mGFAPcre) to ablate astroglial CXCL10 synthesis. These mice, and littermate controls, were immunized with myelin oligodendrocyte glycoprotein peptide 35-55 (MOG peptide) to induce experimental autoimmune encephalomyelitis (EAE). In comparison to the control mice, spinal cord CXCL10 mRNA and protein were sharply diminished in the mGFAPcre/CXCL10fl/fl EAE mice, confirming that astroglia are chiefly responsible for EAE-induced CNS CXCL10 synthesis. Astroglial CXCL10 deletion did not significantly alter the overall composition of CD4+ lymphocytes and CD11b+ cells in the acutely inflamed CNS, but did diminish accumulation of CD4+ lymphocytes in the spinal cord perivascular spaces. Furthermore, IBA1+ microglia/macrophage accumulation within the lesions was not affected by CXCL10 deletion. Clinical deficits were milder and acute demyelination was substantially reduced in the astroglial CXCL10-deleted EAE mice, but long-term axon loss was equally severe in the two groups. We concluded that astroglial CXCL10 enhances spinal cord perivascular CD4+ lymphocyte accumulation and acute spinal cord demyelination in MOG peptide EAE, but does not play an important role in progressive axon loss in this MS model.

Indexed as

AnimalsAstrocytesAxonsCalcium-Binding ProteinsCentral Nervous SystemChemokine CXCL10Disease Models, AnimalDisease ProgressionEncephalomyelitis, Autoimmune, ExperimentalGlial Fibrillary Acidic ProteinLeukocytesLymph NodesMiceMice, Inbred C57BLMice, KnockoutMicrofilament ProteinsAif1 protein, mouseCalcium-Binding ProteinsChemokine CXCL10Cxcl10 protein, mouseGlial Fibrillary Acidic ProteinMicrofilament ProteinsMyelin Basic ProteinMyelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Peptide Fragments

Identifiers

PMID24924222
PMCPMC4066277
OpenAlexW2079770437

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.