Evidence map›Paper›PMID 21507985›Full record

ArticleJournal of virology2011

CXCR3-dependent plasma blast migration to the central nervous system during viral encephalomyelitis.

Cristina P Marques, Parul Kapil, David R Hinton, Claudia Hindinger, Stephen L Nutt, Richard M Ransohoff, Timothy W Phares, Stephen A Stohlman, Cornelia C Bergmann

Abstract read
In one paragraph

Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

53 citing papers in PubMed, 67 citations in OpenAlex.

  1. B cell-intrinsic CXCR3 drives efficient generation of ectopic pulmonary germinal center responses to influenza A virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

9 authors at 3 institutions in 2 countries.

Cristina P MarquesDepartment of Neuroscience, Lerner Research Institute, The Cleveland Clinic, 9500 Euclid Avenue, NC30, Cleveland, OH 44195, USA.
Parul Kapil
David R Hinton
Claudia Hindinger
Stephen L Nutt
Richard M Ransohoff
Timothy W Phares
Stephen A Stohlman
Cornelia C Bergmann
Cleveland Clinic Lerner College of Medicine · USUniversity of Southern California · USWalter and Eliza Hall Institute of Medical Research · AU

Funding

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 AI047249
6 · The paper itself

Abstract

Immunoglobulin in cerebral spinal fluid and antibody secreting cells (ASC) within the central nervous system (CNS) parenchyma are common hallmarks of microbial infections and autoimmune disorders. However, the signals directing ASC migration into the inflamed CNS are poorly characterized. This study demonstrates that CXCR3 mediates CNS accumulation of ASC during neurotropic coronavirus-induced encephalomyelitis. Expansion of CXCR3-expressing ASC in draining lymph nodes prior to accumulation within the CNS was consistent with their recruitment by sustained expression of CXCR3 ligands during viral persistence. Both total and virus-specific ASC were reduced greater than 80% in the CNS of infected CXCR3(-/-) mice. Similar T cell CNS recruitment and local T cell-dependent antiviral activity further indicated that the ASC migration defect was T cell independent. Furthermore, in contrast to the reduction of ASC in the CNS, neither virus-specific ASC trafficking to bone marrow nor antiviral serum antibody was reduced relative to levels in control mice. Impaired ASC recruitment into the CNS of infected CXCR3(-/-) mice coincided with elevated levels of persisting viral RNA, sustained infectious virus, increased clinical disease, and mortality. These results demonstrate that CXCR3 ligands are indispensable for recruitment of activated ASC into the inflamed CNS and highlight their local protective role during persistent infection.

Indexed as

AnimalsCell MovementCentral Nervous SystemCoronavirus InfectionsEncephalomyelitisFemaleMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMurine hepatitis virusPlasma CellsReceptors, CXCR3Receptors, CXCR3

Identifiers

PMID21507985
PMCPMC3126522
OpenAlexW2171428877

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.