Evidence map›Paper›PMID 30109979›Full record

ReviewViral immunology

Chemokine CXCL10 and Coronavirus-Induced Neurologic Disease.

Dominic Skinner, Brett S Marro, Thomas E Lane

Open access · greenAbstract readReview
In one paragraph

Review in Viral immunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 51 citations in OpenAlex.

  1. Characterization of an isogenicInfection and immunity · 2026
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  15. Neuroinflammation: A Signature or a Cause of Epilepsy?International journal of molecular sciences · 2021
    Review
  16. Article
  17. 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

3 authors at 2 institutions in 1 country.

Dominic Skinner1 Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah.
Brett S Marro2 Department of Molecular Biology and Biochemistry, University of California, Irvine, Irvine, California.
Thomas E Lane1 Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah.
University of Utah · USUniversity of California, Irvine · US

Funding

Chemokines and Viral-Induced Neurologic DiseaseR01NS041249 · NINDS · UNIVERSITY OF UTAH · PI LANE, THOMAS E · 2002 to 2019
$5.4M
Viral-induced axonopathy: mechanisms of damage and repairR01NS091939 · NINDS · UNIVERSITY OF UTAH · PI FUJINAMI, ROBERT S, LANE, THOMAS E · 2016 to 2020
$1.7M
NINDS NIH HHS R01 NS041249NINDS NIH HHS R01 NS091939
6 · The paper itself

Abstract

Chemokines (chemotactic cytokines) are involved in a wide variety of biological processes. Following microbial infection, there is often robust chemokine signaling elicited from infected cells, which contributes to both innate and adaptive immune responses that control growth of the invading pathogen. Infection of the central nervous system (CNS) by the neuroadapted John Howard Mueller (JHM) strain of mouse hepatitis virus (JHMV) provides an excellent example of how chemokines aid in host defense as well as contribute to disease. Intracranial inoculation of the CNS of susceptible mice with JHMV results in an acute encephalomyelitis characterized by widespread dissemination of virus throughout the parenchyma. Virus-specific T cells are recruited to the CNS, and control viral replication through release of antiviral cytokines and cytolytic activity. Sterile immunity is not acquired, and virus will persist primarily in white matter tracts leading to chronic neuroinflammation and demyelination. Chemokines are expressed and contribute to defense as well as chronic disease by attracting targeted populations of leukocytes to the CNS. The T cell chemoattractant chemokine CXCL10 (interferon-inducible protein 10 kDa, IP-10) is prominently expressed in both stages of disease, and serves to attract activated T and B lymphocytes expressing CXC chemokine receptor 3 (CXCR3), the receptor for CXCL10. Functional studies that have blocked expression of either CXCL10 or CXCR3 illuminate the important role of this signaling pathway in host defense and neurodegeneration in a model of viral-induced neurologic disease.

Indexed as

AnimalsCentral Nervous System Viral DiseasesChemokine CXCL10Chemotactic FactorsCoronavirus InfectionsDemyelinating DiseasesHumansMiceMice, Inbred C57BLMurine hepatitis virusReceptors, CXCR3Signal TransductionT-LymphocytesChemokine CXCL10Chemotactic FactorsCxcr3 protein, mouseReceptors, CXCR3CNS infectioncoronavirusCXCL10

Identifiers

PMID30109979
PMCPMC6350065
OpenAlexW2885781318

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.