Evidence map›Paper›PMID 24942687›Full record

ReviewImmunological reviews2014

Directing traffic: IL-17 and IL-22 coordinate pulmonary immune defense.

Jeremy P McAleer, Jay K Kolls

Open access · greenAbstract readReview
In one paragraph

Review in Immunological reviews, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed
10.5field-weighted citation impact, top 1% 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

116 citing papers in PubMed, 187 citations in OpenAlex.

  1. Trial
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  10. Sputum Cytokine Repeatability in COPD.International journal of chronic obstructive pulmonary disease · 2025
    Article
  11. Article
  12. I don't know about you, but I'm feeling IL-22.Cytokine & growth factor reviews · 2024
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

56 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

2 authors at 1 institution in 1 country.

Jeremy P McAleerRichard King Mellon Foundation Institute for Pediatric Research, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, PA, USA.
Jay K Kolls
Richard King Mellon Foundation · US

Funding

Th17 Cytokines and Lung ImmunityR37HL079142 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KOLLS, JAY K · 2010 to 2017
$3.6M
Synergy between TLR2 and IL-22R in airway epithelial cells during MRSA challengeF32AI096772 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MCALEER, JEREMY P. · 2011 to 2013
$147k
NHLBI NIH HHS R37 HL079142NHLBI NIH HHS R37-HL079142NIAID NIH HHS F32 AI096772NIAID NIH HHS F32AI096772
6 · The paper itself

Abstract

Respiratory infections and diseases are among the leading causes of death worldwide, and effective treatments probably require manipulating the inflammatory response to pathogenic microbes or allergens. Here, we review mechanisms controlling the production and functions of interleukin-17 (IL-17) and IL-22, cytokines that direct several aspects of lung immunity. Innate lymphocytes (γδ T cells, natural killer cells, innate lymphoid cells) are the major source of IL-17 and IL-22 during acute infections, while CD4(+) T-helper 17 (Th17) cells contribute to vaccine-induced immunity. The characterization of dendritic cell (DC) subsets has revealed their central roles in T-cell activation. CD11b(+) DCs stimulated with bacteria or fungi secrete IL-1β and IL-23, potent inducers of IL-17 and IL-22. On the other hand, recognition of viruses by plasmacytoid DCs inhibits IL-1β and IL-23 release, increasing susceptibility to bacterial superinfections. IL-17 and IL-22 primarily act on the lung epithelium, inducing antimicrobial proteins and neutrophil chemoattractants. Recent studies found that stimulation of macrophages and DCs with IL-17 also contributes to antibacterial immunity, while IL-22 promotes epithelial proliferation and repair following injury. Chronic diseases such as asthma and chronic obstructive pulmonary disease have been associated with IL-17 and IL-22 responses directed against innocuous antigens. Future studies will evaluate the therapeutic efficacy of targeting the IL-17/IL-22 pathway in pulmonary inflammation.

Indexed as

Adaptive ImmunityAnimalsAsthmaDendritic CellsHost-Pathogen InteractionsHumansImmunity, InnateInflammationInterleukin-17Interleukin-22InterleukinsLungMicrobiotaReceptors, InterleukinReceptors, Interleukin-17Respiratory MucosaInterleukin-17Interleukin-22interleukin-22 receptorInterleukinsReceptors, InterleukinReceptors, Interleukin-17VaccinesIL-17IL-22immunitylungT cell

Identifiers

PMID24942687
PMCPMC4066195
OpenAlexW2152011851

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.