Evidence map›Paper›PMID 25548251›Full record

ReviewJournal of leukocyte biology2015

Cytokine crowdsourcing: multicellular production of TH17-associated cytokines.

Kathleen O Busman-Sahay, Travis Walrath, Samuel Huber, William O'Connor

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of leukocyte biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  4. Review
  5. Review
  6. Article
  7. Frontiers in cellular and infection microbiology · 2020
    Article
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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 2 institutions in 2 countries.

Kathleen O Busman-Sahay*Center for Immunology and Microbial Disease, Albany Medical Center, Albany, New York, USA; and Department of Internal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Travis Walrath*Center for Immunology and Microbial Disease, Albany Medical Center, Albany, New York, USA; and Department of Internal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Samuel Huber*Center for Immunology and Microbial Disease, Albany Medical Center, Albany, New York, USA; and Department of Internal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
William O'Connor*Center for Immunology and Microbial Disease, Albany Medical Center, Albany, New York, USA; and Department of Internal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany oconnow@mail.amc.edu.
Albany Medical Center Hospital · USUniversität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the 2 decades since its discovery, IL-17A has become appreciated for mounting robust, protective responses against bacterial and fungal pathogens. When improperly regulated, however, IL-17A can play a profoundly pathogenic role in perpetuating inflammation and has been linked to a wide variety of debilitating diseases. IL-17A is often present in a composite milieu that includes cytokines produced by TH17 cells (i.e., IL-17F, IL-21, IL-22, and IL-26) or associated with other T cell lineages (e.g., IFN-γ). These combinatorial effects add mechanistic complexity and more importantly, contribute differentially to disease outcome. Whereas TH17 cells are among the best-understood cell types that secrete IL-17A, they are frequently neither the earliest nor dominant producers. Indeed, non-TH17 cell sources of IL-17A can dramatically alter the course and severity of inflammatory episodes. The dissection of the temporal regulation of TH17-associated cytokines and the resulting net signaling outcomes will be critical toward understanding the increasingly intricate role of IL-17A and TH17-associated cytokines in disease, informing our therapeutic decisions. Herein, we discuss important non-TH17 cell sources of IL-17A and other TH17-associated cytokines relevant to inflammatory events in mucosal tissues.

Indexed as

AnimalsCytokinesHumansInterleukin-17Models, ImmunologicalTh17 CellsCytokinesInterleukin-17IL-17AIL-17FIL-17RAIL-22inflammationmucosal

Identifiers

PMID25548251
PMCPMC5477895
OpenAlexW2115810118

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.