Evidence map›Paper›PMID 21478401›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

An aberrant thymus in CCR5-/- mice is coupled with an enhanced adaptive immune response in fungal infection.

Danielle N Kroetz, George S Deepe

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

  1. CCR5 marks a subset of mouse hematopoietic stem cells that are myeloid primed and expand with age.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Adaptive immunity to fungi.Annual review of immunology · 2012
    Review
  13. Regulatory T cells in infection.Advances in immunology · 2011
    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

2 authors at 2 institutions in 2 countries.

Danielle N KroetzDepartment of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
George S Deepe
Department of Veterans Affairs · AUUniversity of Cincinnati Medical Center · US

Funding

Immunopathogenesis in HistoplasmosisR01AI073337 · NIAID · UNIVERSITY OF CINCINNATI · PI DEEPE, GEORGE S. · 2008 to 2012
$2.0M
Chemokine-Cytokine Nexus in Fungal ImmunityR01AI083313 · NIAID · UNIVERSITY OF CINCINNATI · PI DEEPE, GEORGE S. · 2010 to 2014
$1.9M
Chemokine-Cytokine Nexus in Fungal ImmunityR56AI083313 · NIAID · UNIVERSITY OF CINCINNATI · PI DEEPE, GEORGE S. · 2009 to 2009
$294k
NIAID NIH HHS AI-07337NIAID NIH HHS AI-083313NIAID NIH HHS R01 AI073337NIAID NIH HHS R01 AI083313NIAID NIH HHS R56 AI083313
6 · The paper itself

Abstract

CCR5 is a potent mediator of regulatory T cell (Treg) chemotaxis. In murine histoplasmosis, mice lacking CCR5 or endogenous CCL4 have a reduced number of Tregs in the lungs, which results in accelerated resolution of infection. In this study, we demonstrate that CCR5 controls the outcome of Histoplasma capsulatum infection by dictating thymic and lymph node egress of Tregs. Mice lacking CCR5 or treated with a mAb to CCL4 had more Tregs in the thymus prior to and during infection. Thymic accumulation was associated with diminished transcription of the sphingosine 1-phosphate 1 receptor and Krüppel-like factor 2, both of which regulate thymic and lymph node emigration of T cells. The significance of CCR5 in Treg egress was demonstrated by generating mixed bone marrow chimeras. Chimeric mice had an increased proportion of CCR5(-/-) Tregs in the thymus and lymph nodes and a decreased proportion of Tregs in the lungs prior to and during H. capsulatum infection. Hence, CCR5 signaling regulates pathogen persistence in murine histoplasmosis by regulating Tregs exiting from the thymus and lymph nodes and, consequently, their subsequent homing in the periphery.

Indexed as

Adaptive ImmunityAnimalsCell MovementChemokine CCL4HistoplasmaHistoplasmosisKruppel-Like Transcription FactorsLungLung Diseases, FungalMiceMice, Inbred C57BLMice, KnockoutPolymerase Chain ReactionRadiation ChimeraReceptors, CCR5Receptors, LysosphingolipidChemokine CCL4Klf2 protein, mouseKruppel-Like Transcription FactorsReceptors, CCR5Receptors, Lysosphingolipid

Identifiers

PMID21478401
PMCPMC3111447
OpenAlexW1849922370

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.