Evidence map›Paper›PMID 22782966›Full record

ReviewJournal of leukocyte biology2012

Regulation of inflammation by interleukin-4: a review of "alternatives".

Irina G Luzina, Achsah D Keegan, Nicola M Heller, Graham A W Rook, Terez Shea-Donohue, Sergei P Atamas

Abstract readReview
In one paragraph

Review in Journal of leukocyte biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 167 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
167citing papers in PubMed, 5 pooled it
6.6field-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

167 citing papers in PubMed, 5 syntheses or guidelines pooled it, 349 citations in OpenAlex.

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107 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

6 authors at 4 institutions in 2 countries.

Irina G LuzinaUniversity of Maryland School of Medicine, Baltimore, MD 21201, USA.
Achsah D Keegan
Nicola M Heller
Graham A W Rook
Terez Shea-Donohue
Sergei P Atamas
Baltimore VA Medical Center · USUniversity of Maryland, Baltimore · USJohns Hopkins University · USUniversity College London · GB

Funding

Molecular Mechanisms of IL-4 and IL-13 SignalingR01AI038985 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI KEEGAN, ACHSAH D. · 2001 to 2010
$3.7M
GI Nematodes and Gut Functional Responses to InflammationR01AI049316 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI SHEA-DONOHUE, TEREZ · 2002 to 2012
$3.6M
IRS phosphorylation by type I IL-4R signaling and its role in allergic diseaseR00HL096897 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI HELLER, NICOLA M · 2011 to 2013
$781k
A Novel Model of, and Pre-clinical Therapy for, Scleroderma Lung DiseaseR21HL106196 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI ATAMAS, SERGEI P. · 2011 to 2012
$422k
INTEGRIN-DEPENDENT T CELL-MEDIATED MECHANISMS OF PULMONARY FIBROSISR03AR054946 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI LUZINA, IRINA G. · 2008 to 2010
$224k
Unique immune regulation by alternatively spliced interleukin-4I01CX000107 · VA · BALTIMORE VA MEDICAL CENTER · PI ATAMAS, SERGEI P. · 2011 to 2014
–
Integrin-dependent mechanism of T cell-mediated pulmonary fibrosisI01CX000101 · VA · BALTIMORE VA MEDICAL CENTER · PI LUZINA, IRINA G. · 2009 to 2017
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CSRD VA I01 CX000101CSRD VA I01 CX000107NHLBI NIH HHS 1R21HL106196NHLBI NIH HHS R00 HL096897NHLBI NIH HHS R21 HL106196NIAID NIH HHS 2R01AI049316NIAID NIH HHS R01 AI038985NIAID NIH HHS R01AI038985NIAID NIH HHS R01 AI049316NIAMS NIH HHS 1R03AR054946NIAMS NIH HHS R03 AR054946
6 · The paper itself

Abstract

Studies of IL-4 have revealed a wealth of information on the diverse roles of this cytokine in homeostatic regulation and disease pathogenesis. Recent data suggest that instead of simple linear regulatory pathways, IL-4 drives regulation that is full of alternatives. In addition to the well-known dichotomous regulation of Th cell differentiation by IL-4, this cytokine is engaged in several other alternative pathways. Its own production involves alternative mRNA splicing, yielding at least two functional isoforms: full-length IL-4, encoded by the IL-4 gene exons 1-4, and IL-4δ2, encoded by exons 1, 3, and 4. The functional effects of these two isoforms are in some ways similar but in other ways quite distinct. When binding to the surface of target cells, IL-4 may differentially engage two different types of receptors. By acting on macrophages, a cell type critically involved in inflammation, IL-4 induces the so-called alternative macrophage activation. In this review, recent advances in understanding these three IL-4-related branch points--alternative splicing of IL-4, differential receptor engagement by IL-4, and differential regulation of macrophage activation by IL-4--are summarized in light of their contributions to inflammation.

Indexed as

AnimalsAsthmaHumansInflammationInterleukin-4Macrophage ActivationProtein Tyrosine Phosphatase, Non-Receptor Type 6Receptors, Interleukin-13Receptors, Interleukin-4Scleroderma, SystemicSignal TransductionTuberculosisInterleukin-4Protein Tyrosine Phosphatase, Non-Receptor Type 6Receptors, Interleukin-13Receptors, Interleukin-4

Identifiers

PMID22782966
PMCPMC3441310
OpenAlexW2103125300

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.