Evidence map›Paper›PMID 22504650›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

B cell-specific S1PR1 deficiency blocks prion dissemination between secondary lymphoid organs.

Simon W F Mok, Richard L Proia, Volker Brinkmann, Neil A Mabbott

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Experimental inoculation of CD11cAccess microbiology · 2020
    Article
  2. Article
  3. How do PrPPathogens (Basel, Switzerland) · 2017
    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

4 authors at 3 institutions in 3 countries.

Simon W F MokThe Roslin Institute and Royal (Dick) School of Veterinary Sciences, University of Edinburgh, Midlothian EH25 9RG, United Kingdom.
Richard L Proia
Volker Brinkmann
Neil A Mabbott
University of Edinburgh · GBNational Institute of Diabetes and Digestive and Kidney Diseases · USNovartis (Switzerland) · CH

Funding

Sphingolipid Biology of NeurodegenerationZIADK056016 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI PROIA, RICHARD · 2009 to 2025
$21.3M
Mouse Models of Novel Sphingolipid Biology and Disease MechanismsZIADK056014 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI PROIA, RICHARD · 2009 to 2025
$10.6M
Sphingolipid Biology of Inflammation and ImmunityZIADK056015 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI PROIA, RICHARD · 2009 to 2021
$7.9M
Biotechnology and Biological Sciences Research Council BB/D00831X/1Biotechnology and Biological Sciences Research Council BB/D00831X/2Biotechnology and Biological Sciences Research Council BB/D00831X/3Biotechnology and Biological Sciences Research Council BBS/E/D/05241339Biotechnology and Biological Sciences Research Council BBS/E/D/20251967Biotechnology and Biological Sciences Research Council BBS/E/D/20251968Intramural NIH HHSMedical Research Council G0700640Medical Research Council G0700640(81544)
6 · The paper itself

Abstract

Many prion diseases are peripherally acquired (e.g., orally or via lesions to skin or mucous membranes). After peripheral exposure, prions replicate first upon follicular dendritic cells (FDC) in the draining lymphoid tissue before infecting the brain. However, after replication upon FDC within the draining lymphoid tissue, prions are subsequently propagated to most nondraining secondary lymphoid organs (SLO), including the spleen, by a previously underdetermined mechanism. The germinal centers in which FDC are situated produce a population of B cells that can recirculate between SLO. Therefore, we reasoned that B cells were ideal candidates by which prion dissemination between SLO may occur. Sphingosine 1-phosphate receptor (S1PR)1 stimulation controls the egress of T and B cells from SLO. S1PR1 signaling blockade sequesters lymphocytes within SLO, resulting in lymphopenia in the blood and lymph. We show that, in mice treated with the S1PR modulator FTY720 or with S1PR1 deficiency restricted to B cells, the dissemination of prions from the draining lymph node to nondraining SLO is blocked. These data suggest that B cells interacting with and acquiring surface proteins from FDC and recirculating between SLO via the blood and lymph mediate the initial propagation of prions from the draining lymphoid tissue to peripheral tissues.

Indexed as

Epitopes, B-LymphocyteAnimalsB-Lymphocyte SubsetsLymphoid TissueMicePrPSc ProteinsReceptors, LysosphingolipidScrapieSphingosine-1-Phosphate ReceptorsEpitopes, B-LymphocytePrPSc ProteinsReceptors, LysosphingolipidS1pr1 protein, mouseSphingosine-1-Phosphate Receptors

Identifiers

PMID22504650
PMCPMC3364719
OpenAlexW2158770661

What OpenQuestion holds

Textmetadata
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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.