Evidence map›Paper›PMID 29563123›Full record

ArticleBlood advances2018

Murine CMV induces type 1 IFN that impairs differentiation of MDSCs critical for transplantation tolerance.

Anil Dangi, Lei Zhang, Xiaomin Zhang, Xunrong Luo

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-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

15 citing papers in PubMed, 17 citations in OpenAlex.

  1. Mechanisms and Determinants of CMV Reactivation in Kidney Transplantation.International journal of molecular sciences · 2026
    Review
  2. Review
  3. Review
  4. Acute murine cytomegalovirus disrupts established transplantation tolerance and causes recipient allo-sensitization.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2021
    Article
  5. Article
  6. Apoptotic Donor Cells in Transplantation.Frontiers in immunology · 2021
    Review
  7. Article
  8. Review
  9. Review
  10. Resilience of T cell-intrinsic dysfunction in transplantation tolerance.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Apoptotic cell-based therapies for promoting transplantation tolerance.Current opinion in organ transplantation · 2018
    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

4 authors at 2 institutions in 3 countries.

Anil DangiCenter for Kidney Research and Therapeutics, Feinberg Cardiovascular Research Institute.ORCID 0000-0003-1185-3079
Lei ZhangCenter for Kidney Research and Therapeutics, Feinberg Cardiovascular Research Institute.
Xiaomin ZhangComprehensive Transplant Center, Northwestern University Feinberg School of Medicine, Chicago, IL.
Xunrong LuoCenter for Kidney Research and Therapeutics, Feinberg Cardiovascular Research Institute.ORCID 0000-0001-5581-9409
Cardiovascular Institute Hospital · JPNorthwestern University · US

Funding

Precision Cell Isolation and Analysis CoreP01AI112522 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LUO, XUNRONG · 2015 to 2019
$11.9M
Protein-Releasing Microporous Scaffolds for Cell Replacement TherapyR01EB009910 · NIBIB · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUO, XUNRONG, SHEA, LONNIE D · 2010 to 2018
$3.5M
Modeling concurrent cytomegalovirus infection and transplantation toleranceR01AI114824 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LUO, XUNRONG · 2016 to 2020
$1.4M
NIAID NIH HHS P01 AI112522NIAID NIH HHS R01 AI114824NIBIB NIH HHS R01 EB009910
6 · The paper itself

Abstract

Clinical tolerance without immunosuppression has now been achieved for organ transplantation, and its scope will likely continue to expand. In this context, a previously understudied and now increasingly relevant area is how microbial infections might affect the efficacy of tolerance. A highly prevalent and clinically relevant posttransplant pathogen is cytomegalovirus (CMV). Its impact on transplantation tolerance and graft outcomes is not well defined. Employing a mouse model of CMV (MCMV) infection and allogeneic pancreatic islet transplantation in which donor-specific tolerance was induced by infusing donor splenocytes rendered apoptotic by treatment with ethylenecarbodiimide, we investigated the effect of CMV infection on transplantation tolerance induction. We found that acute MCMV infection abrogated tolerance induction and that this abrogation correlated with an alteration in the differentiation and function of myeloid-derived suppressor cells (MDSCs). These effects on MDSCs were mediated in part through MCMV induced type 1 interferon (IFN) production. During MCMV infection, the highly immunosuppressive Gr1

Indexed as

Transplantation ToleranceAnimalsApoptosisBiomarkersCell DifferentiationCell LineageHerpesviridae InfectionsImmunomodulationInflammation MediatorsInterferon Type IIslets of LangerhansMaleMiceMonocytesMuromegalovirusMyeloid-Derived Suppressor CellsBiomarkersInflammation MediatorsInterferon Type I

Identifiers

PMID29563123
PMCPMC5873231
OpenAlexW2789335593

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.