Evidence map›Paper›PMID 23378430›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

STING/MPYS mediates host defense against Listeria monocytogenes infection by regulating Ly6C(hi) monocyte migration.

Lei Jin, Andrew Getahun, Heather M Knowles, Jennifer Mogan, Linda J Akerlund, Thomas A Packard, Anne-Laure Perraud, John C Cambier

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. 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
1.2field-weighted citation impact, top 22% 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, 58 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. The commoneLife · 2024
    Article
  7. The commonbioRxiv : the preprint server for biology · 2024
    Article
  8. Article
  9. Establishment of aJournal of pathogens · 2024
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. STING Contributes to Host Defense AgainstFrontiers in immunology · 2021
    Article
  17. Article
  18. Article
  19. Review
  20. Review
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

8 authors at 2 institutions in 1 country.

Lei JinIntegrated Department of Immunology, University of Colorado Denver School of Medicine and National Jewish Health, Denver, CO 80206, USA. jinl@mail.amc.edu
Andrew Getahun
Heather M Knowles
Jennifer Mogan
Linda J Akerlund
Thomas A Packard
Anne-Laure Perraud
John C Cambier
National Jewish Health · USUniversity of Colorado Denver · US

Funding

Molecular Mechanisms of Immune ToleranceT32AI074491 · NIAID · NATIONAL JEWISH HEALTH · PI CAMBIER, JOHN C, PELANDA, ROBERTA · 2009 to 2023
$4.1M
NKIP signaling and functionsR01AI062739 · NIAID · NATIONAL JEWISH HEALTH · PI CAMBIER, JOHN C · 2005 to 2009
$2.2M
Mouse modeling of a human STING gene variant for infectious diseaseR21AI099346 · NIAID · UNIVERSITY OF COLORADO DENVER · PI CAMBIER, JOHN C · 2012 to 2013
$410k
NIAID NIH HHS 3R01AI062739-05S2NIAID NIH HHS R01 AI062739NIAID NIH HHS R21 AI099346NIAID NIH HHS T32 AI074491
6 · The paper itself

Abstract

MPYS (also known as STING, MITA, and TMEM173) is a type I IFN stimulator that is essential for host defense against DNA virus infection and appears important in defense against certain bacteria. The in vivo significance and mechanisms by which MPYS mediates host defense against nonviral pathogens are unknown. Using an MPYS-deficient mouse (Tmem173(<tm1Camb>)), we determined that, distinct from the IFNAR(-/-) mice, MPYS deficiency leads to increased bacterial burden in the liver upon Listeria monocytogenes infection. The increase was correlated with the diminished MCP-1 and MCP-3 chemokine production and decreased blood and liver Ly6C(hi) monocyte frequency. We further demonstrate that MPYS-deficient Ly6C(hi) monocytes are intrinsically defective in migration to the liver. Lastly, adoptive transfer of wild-type Ly6C(hi) monocyte into MPYS-deficient mice decreases their liver bacterial burden. Our findings reveal a novel in vivo function of MPYS that is distinct from its role in activating type I IFN production.

Indexed as

AnimalsAntigens, LyCell MovementCells, CulturedDisease Models, AnimalHost-Pathogen InteractionsListeriosisLiverMembrane ProteinsMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutMice, TransgenicMonocytesSpleenAntigens, LyLy-6C antigen, mouseMembrane ProteinsSting1 protein, mouseSTING Protein

Identifiers

PMID23378430
PMCPMC3593745
OpenAlexW2134362254

What OpenQuestion holds

Textmetadata
LicenceTDM
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.