Evidence map›Paper›PMID 12919745›Full record

ArticleVirology2003

Functional analysis of the CC chemokine receptor 5 (CCR5) on virus-specific CD8+ T cells following coronavirus infection of the central nervous system.

William G Glass, Thomas E Lane

Open access · greenAbstract read
In one paragraph

Article in Virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

36 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. AnFrontiers in pharmacology · 2024
    Article
  4. Article
  5. Review
  6. Article
  7. Inflammation, immunity and potential target therapy of SARS-COV-2: A total scale analysis review.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2021
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Chemokine receptor CCR5 correlates with functional CD8FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  13. Review
  14. MicroRNA 155 and viral-induced neuroinflammation.Journal of neuroimmunology · 2017
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  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

2 authors at 1 institution in 1 country.

William G GlassDepartment of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697-3900, USA.
Thomas E Lane
University of California, Irvine · US

Funding

Chemokines and Viral-Induced Neurologic DiseaseR01NS041249 · NINDS · UNIVERSITY OF UTAH · PI LANE, THOMAS E · 2002 to 2019
$5.4M
PATHOLOGICAL MECHANISMS OF DEMYELINATIONR29NS037336 · NINDS · UNIVERSITY OF CALIFORNIA IRVINE · PI LANE, THOMAS E · 1998 to 2002
$325k
NINDS NIH HHS NS37336NINDS NIH HHS NS41249NINDS NIH HHS R01 NS041249PHS HHS A107319-12
6 · The paper itself

Abstract

Intracranial infection of C57BL/6 mice with mouse hepatitis virus (MHV) results in an acute encephalomyelitis followed by a demyelinating disease similar in pathology to the human disease multiple sclerosis (MS). T cells participate in both defense and disease progression following MHV infection. Expression of chemokine receptors on activated T cells is important in allowing these cells to traffic into and accumulate within the central nervous system (CNS) of MHV-infected mice. The present study evaluated the contributions of CCR5 to the activation and trafficking of virus-specific CD8(+) T cells into the MHV-infected CNS mice. Comparable numbers of virus-specific CD8(+) T cells derived from immunized CCR5(+/+) or CCR5(-/-) mice were present within the CNS of MHV-infected RAG1(-/-) mice following adoptive transfer, indicating that CCR5 is not required for trafficking of these cells into the CNS. RAG1(-/-) recipients of CCR5(-/-)-derived CD8(+) T cells exhibited a modest, yet significant (P </= 0.05), reduction in viral burden within the brain which correlated with increased CTL activity and IFN-gamma expression. Histological analysis of RAG1(-/-) recipients of either CCR5(+/+)or CCR5(-/-)-derived CD8(+) T cells revealed only focal areas of demyelination with no significant differences in white matter destruction. These data indicate that CCR5 signaling on CD8(+) T cells modulates antiviral activities but is not essential for entry into the CNS.

Indexed as

Adoptive TransferAnimalsBrainCD8-Positive T-LymphocytesCoronavirus InfectionsInterferon-gammaMiceMice, Inbred C57BLMice, Inbred StrainsMurine hepatitis virusReceptors, CCR5Interferon-gammaReceptors, CCR5

Identifiers

PMID12919745
PMCPMC7127441
OpenAlexW1986804060

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.