Evidence map›Paper›PMID 23302888›Full record

ArticleJournal of virology2013

Astrocyte-derived CXCL10 drives accumulation of antibody-secreting cells in the central nervous system during viral encephalomyelitis.

Timothy W Phares, Stephen A Stohlman, David R Hinton, Cornelia C Bergmann

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
3.0field-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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Pooled it
  2. Article
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  5. Article
  6. Article
  7. Unraveling the complexities of neurotropic virus infection and immune evasion.Microbiology and molecular biology reviews : MMBR · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Nucleotide metabolism, leukodystrophies, and CNS pathology.Journal of inherited metabolic disease · 2024
    Review
  15. Article
  16. Article
  17. Article
  18. Article
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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

4 authors at 2 institutions in 1 country.

Timothy W PharesDepartment of Neurosciences, Lerner Research Institute, The Cleveland Clinic, Cleveland, OH, USA.
Stephen A Stohlman
David R Hinton
Cornelia C Bergmann
Cleveland Clinic Lerner College of Medicine · USUniversity of Southern California · US

Funding

T Cell Dependent Regulation of Viral PersistenceP01NS064932 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI BERGMANN, CORNELIA · 2009 to 2013
$7.9M
Immune Regulation of CNS Viral RecrudescenceR01AI047249 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BERGMANN, CORNELIA · 2001 to 2010
$3.1M
Immune Regulation of Viral RecrudescenceR56AI047249 · NIAID · CLEVELAND CLINIC LERNER COM-CWRU · PI BERGMANN, CORNELIA · 2012 to 2012
$393k
NIAID NIH HHS AI 47249NIAID NIH HHS R01 AI047249NIAID NIH HHS R56 AI047249NIAID NIH HHS R56AI047249NINDS NIH HHS NS064932NINDS NIH HHS P01 NS064932
6 · The paper itself

Abstract

Microbial infections of the central nervous system (CNS) are often associated with local accumulation of antibody (Ab)-secreting cells (ASC). By providing a source of Ab at the site of infection, CNS-localized ASC play a critical role in acute viral control and in preventing viral recrudescence. Following coronavirus-induced encephalomyelitis, the CNS accumulation of ASC is chemokine (C-X-C motif) receptor 3 (CXCR3) dependent. This study demonstrates that CNS-expressed CXCR3 ligand CXCL10 is the critical chemokine regulating ASC accumulation. Impaired ASC recruitment in CXCL10(-/-) but not CXCL9(-/-) mice was consistent with reduced CNS IgG and κ-light chain mRNA and virus-specific Ab. Moreover, the few ASC recruited to the CNS in CXCL10(-/-) mice were confined to the vasculature, distinct from the parenchymal localization in wild-type and CXCL9(-/-) mice. However, neither CXCL9 nor CXCL10 deficiency diminished neutralizing serum Ab, supporting a direct role for CXCL10 in ASC migration. T cell accumulation, localization, and effector functions were also not affected in either CXCL9(-/-) or CXCL10(-/-) mice, consistent with similar control of infectious virus. There was also no evidence for dysregulation of chemokines or cytokines involved in ASC regulation. The distinct roles of CXCL9 and CXCL10 in ASC accumulation rather coincided with their differential localization. While CXCL10 was predominantly expressed by astrocytes, CXCL9 expression was confined to the vasculature/perivascular spaces. These results suggest that CXCL10 is critical for two phases: recruitment of ASC to the CNS vasculature and ASC entry into the CNS parenchyma.

Indexed as

Cell MovementAnimalsAntibody-Producing CellsAstrocytesChemokine CXCL10CoronavirusCoronavirus InfectionsEncephalomyelitisMiceMice, Inbred C57BLMice, KnockoutChemokine CXCL10Cxcl10 protein, mouse

Identifiers

PMID23302888
PMCPMC3592145
OpenAlexW2121143460

What OpenQuestion holds

Textmetadata
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.