Evidence map›Paper›PMID 29447279›Full record

ReviewPLoS pathogens2018

Regulatory T cells in retroviral infections.

Kim J Hasenkrug, Claire A Chougnet, Ulf Dittmer

Open access · goldAbstract readReview
In one paragraph

Review in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

33 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Cell therapies for viral diseases: a new frontier.Seminars in immunopathology · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. T-Follicular-Like CD8Frontiers in immunology · 2022
    Article
  17. High-frequency and activation of CD4Veterinary research · 2021
    Article
  18. Article
  19. Article
  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

3 authors at 2 institutions in 2 countries.

Kim J HasenkrugRocky Mountain Laboratories, NIAID, NIH, Hamilton, Montana, United States of America.ORCID 0000-0001-8523-4911
Claire A ChougnetDivision of Immunobiology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, United States of America.
Ulf DittmerInstitute for Virology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.ORCID 0000-0001-9284-4849
Cincinnati Children's Hospital Medical Center · USUniversity of Duisburg-Essen · DE

Funding

Immunology And Pathology Of Acute Murine Leukemia Virus InfectionsZIAAI000753 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI HASENKRUG, KIM · 2009 to 2022
$8.1M
HIV Infection in Humanized MiceZIAAI001141 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI HASENKRUG, KIM · 2011 to 2019
$4.2M
Homeostasis and function of regulatory T cells in agingR01AG033057 · NIA · CINCINNATI CHILDRENS HOSP MED CTR · PI CHOUGNET, CLAIRE A., HILDEMAN, DAVID A · 2009 to 2018
$3.5M
Direct interactions with HDL promote regulatory T cells survivalR21AI128218 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI CHOUGNET, CLAIRE A. · 2017 to 2018
$445k
NIAID NIH HHS R21 AI128218NIA NIH HHS R01 AG033057NIH HHS R21AI128218
6 · The paper itself

Abstract

Tight regulation of immune responses is not only critical for preventing autoimmune diseases but also for preventing immunopathological damage during infections in which overactive immune responses may be more harmful for the host than the pathogen itself. Regulatory T cells (Tregs) play a critical role in this regulation, which was discovered using the Friend retrovirus (FV) mouse model. Subsequent FV studies revealed basic biological information about Tregs, including their suppressive activity on effector cells as well as the molecular mechanisms of virus-induced Treg expansion. Treg suppression not only limits immunopathology but also prevents complete elimination of pathogens contributing to chronic infections. Therefore, Tregs play a complex role in the pathogenesis of persistent retroviral infections. New therapeutic concepts to reactivate effector T-cell responses in chronic viral infections by manipulating Tregs also came from work with the FV model. This knowledge initiated many studies to characterize the role of Tregs in HIV pathogenesis in humans, where a complex picture is emerging. On one hand, Tregs suppress HIV-specific effector T-cell responses and are themselves targets of infection, but on the other hand, Tregs suppress HIV-induced immune hyperactivation and thus slow the infection of conventional CD4+ T cells and limit immunopathology. In this review, the basic findings from the FV mouse model are put into perspective with clinical and basic research from HIV studies. In addition, the few Treg studies performed in the simian immunodeficiency virus (SIV) monkey model will also be discussed. The review provides a comprehensive picture of the diverse role of Tregs in different retroviral infections and possible therapeutic approaches to treat retroviral chronicity and pathogenesis by manipulating Treg responses.

Indexed as

Host-Pathogen InteractionsModels, ImmunologicalAnimalsHumansImmune ToleranceImmunosuppression TherapyLymphopoiesisRetroviridaeRetroviridae InfectionsT-Lymphocytes, Regulatory

Identifiers

PMID29447279
PMCPMC5814043
OpenAlexW2788286532

What OpenQuestion holds

Textmetadata
LicenceCC0
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.