Evidence map›Paper›PMID 21359196›Full record

ArticlePloS one2011

Role of IL-17A on resolution of pulmonary C. neoformans infection.

Karen L Wozniak, Sarah E Hardison, Jay K Kolls, Floyd L Wormley

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

65 citing papers in PubMed, 91 citations in OpenAlex.

  1. Trial
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  10. Macrophage Mediated Immunomodulation DuringFrontiers in cellular and infection microbiology · 2022
    Review
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  14. Article
  15. Article
  16. Animal Models ofFrontiers in immunology · 2020
    Review
  17. Article
  18. Article
  19. Article
  20. Interactions of Cryptococcus with Dendritic Cells.Journal of fungi (Basel, Switzerland) · 2018
    Review

5 more citing papers are in PubMed but not listed here.

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 1 country.

Karen L WozniakDepartment of Biology, The University of Texas at San Antonio, San Antonio, Texas, United States of America. Karen.Wozniak@utsa.edu
Sarah E Hardison
Jay K Kolls
Floyd L Wormley
The University of Texas at San Antonio · USLouisiana State University Health Sciences Center New Orleans · USTexas Center for Infectious Disease · US

Funding

Protective Host Immunity Against Pulmonary CryptococcosisR01AI071752 · NIAID · UNIVERSITY OF TEXAS SAN ANTONIO · PI WORMLEY, FLOYD L. · 2007 to 2018
$3.7M
NON CD4 HOST DEFENSE AGAINST P CARINII PNEUMONIAR01HL061271 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KOLLS, JAY K · 1999 to 2013
$3.6M
IL-23 / Il-17 and Lung Host DefenseR01HL079142 · NHLBI · LSU HEALTH SCIENCES CENTER · PI KOLLS, JAY K · 2005 to 2009
$1.9M
NHLBI NIH HHS R01 HL061271NHLBI NIH HHS R01 HL079142NIAID NIH HHS R01 AI071752NIAID NIH HHS R01 AI071752-03
6 · The paper itself

Abstract

The current studies evaluated the role of interleukin (IL)-17A in the induction of protective immunity against pulmonary cryptococcosis in mice. Protection against pulmonary infection with C. neoformans strain H99γ was associated with increased IL-17A production. Signaling through the IFN-γ receptor (R) was required for increased IL-17A production, however, a Th17-type cytokine profile was not observed. Neutrophils were found to be the predominant leukocytic source of IL-17A, rather than T cells, suggesting that the IL-17A produced was not part of a T cell-mediated Th17-type immune response. Depletion of IL-17A in mice during pulmonary infection with C. neoformans strain H99γ resulted in an initial increase in pulmonary fungal burden, but had no effect on cryptococcal burden at later time points. Also, depletion of IL-17A did not affect the local production of other cytokines. IL-17RA⁻/⁻ mice infected with C. neoformans strain H99γ survived the primary infection as well as a secondary challenge with wild-type cryptococci. However, dissemination of the wild-type strain to the brain was noted in the surviving IL-17RA⁻/⁻ mice. Altogether, our results suggested that IL-17A may be important for optimal protective immune responsiveness during pulmonary C. neoformans infection, but protective Th1-type immune responses are sufficient for protection against cryptococcal infection.

Indexed as

AnimalsChemotaxis, LeukocyteCryptococcosisCryptococcus neoformansCytoprotectionFemaleImmunity, CellularInterleukin-17LungLung Diseases, FungalMiceMice, Inbred BALB CMice, KnockoutTh17 CellsTh1 CellsInterleukin-17

Identifiers

PMID21359196
PMCPMC3040760
OpenAlexW2054660434

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.