Evidence map›Paper›PMID 22342846›Full record

ArticleThe American journal of pathology2012

IL-23 dampens the allergic response to Cryptococcus neoformans through IL-17-independent and -dependent mechanisms.

Wendy A Szymczak, Rani S Sellers, Liise-anne Pirofski

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 41 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Mouse Model of Latent Cryptococcal Infection and Reactivation.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  8. Adaptive immunology ofFrontiers in immunology · 2023
    Review
  9. Article
  10. Observational
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. IL-17 in the lung: the good, the bad, and the ugly.American journal of physiology. Lung cellular and molecular physiology · 2018
    Review
  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 1 country.

Wendy A SzymczakDepartment of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York 10461, USA. l.pirofski@einstein.yu.edu
Rani S Sellers
Liise-anne Pirofski
Albert Einstein College of Medicine · USMontefiore Medical Center · US

Funding

WORD PROCESSORP30CA013330 · NCI · YESHIVA UNIVERSITY · PI THOMAS E ROHAN · 1985 to 2026
$111.2M
Immunology/Pathology CoreP30AI051519 · NIAID · YESHIVA UNIVERSITY · PI GOLDSTEIN, HARRIS · 2003 to 2013
$18.6M
VARIABLE GENE USE AND PNEUMOCOCCAL IMMUNITY IN AIDSR01AI045459 · NIAID · YESHIVA UNIVERSITY · PI PIROFSKI, LIISE-ANNE · 2000 to 2010
$3.9M
Human Antibodies to Crytococcus NeoformansR01AI035370 · NIAID · YESHIVA UNIVERSITY · PI PIROFSKI, LIISE-ANNE · 1994 to 2009
$3.3M
NCI NIH HHS P30 CA013330NIAID NIH HHS P30 AI 051519NIAID NIH HHS P30 AI051519NIAID NIH HHS R01 AI035370NIAID NIH HHS R01 AI 35370NIAID NIH HHS R01 AI44347NIAID NIH HHS R01 AI45459PHS HHS 5T32A1007501
6 · The paper itself

Abstract

The cytokines IL-23 and IL-17 have been implicated in resistance to cryptococcal disease, but it is not clear whether IL-23-mediated production of IL-17 promotes fungal containment following pulmonary challenge with Cryptococcus neoformans. We used mice lacking IL-23 (IL-23p19(-/-)) or IL-17RA (IL-17RA(-/-)), and wild type (WT) C57BL/6 mice to examine the IL-23/IL-17 axis after intranasal infection with the C. neoformans strain 52D. The absence of IL-23 or IL-17RA had no effect on pulmonary or brain fungal burden at 1 or 6 weeks after infection. However, survival of IL-23p19(-/-) mice was reduced compared to IL-17RA(-/-) mice. IL-I7 production by CD4 T cells and natural killer T (NKT) cells was impaired in IL-23p19(-/-) lungs, but was not completely abolished. Both IL-23p19(-/-) and IL-17RA(-/-) mice exhibited impaired neutrophil recruitment, increased serum levels of IgE and IgG2b, and increased deposition of YM1/YM2 crystals in the lung, but only IL-23p19(-/-) mice developed persistent lung eosinophilia. Although survival of IL-17RA(-/-) and WT mice was similar after 17 weeks of infection, only surviving IL-17RA(-/-) mice exhibited cryptococcal dissemination to the blood. These data demonstrate that IL-23 dampens the allergic response to cryptococcal infection through IL-17-independent suppression of eosinophil recruitment and IL-17-dependent regulation of antibody production and crystal deposition. Furthermore, IL-23, and to a lesser extent IL-17, contribute to disease resistance.

Indexed as

AnimalsAntibodies, FungalBrainCD4-Positive T-LymphocytesCryptococcosisCryptococcus neoformansCrystallizationDisease Models, AnimalImmunoglobulin EInterleukin-17Interleukin-23Killer Cells, NaturalLeukocytesLungLung Diseases, FungalMaleAntibodies, FungalImmunoglobulin EInterleukin-17Interleukin-23Receptors, Interleukin-17

Identifiers

PMID22342846
PMCPMC3349902
OpenAlexW2166414010

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.