ArticleJournal of leukocyte biology2011
Alternatively spliced variants of interleukin-4 promote inflammation differentially.
Article in Journal of leukocyte biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- Full-length IL-33 augments pulmonary fibrosis in an ST2- and Th2-independent, non-transcriptomic fashion.Cellular immunology · 2023Article
- Effect of genotype on the disease course in idiopathic pulmonary fibrosis despite antifibrotic treatment.Biomedical reports · 2021Article
- Article
- Shifts in macrophage phenotype at the biomaterial interface via IL-4 eluting coatings are associated with improved implant integration.Biomaterials · 2017Article
- Plasma Inflammatory Cytokine IL-4, IL-8, IL-10, and TNF-α Levels Correlate with Pulmonary Function in Patients with Asthma-Chronic Obstructive Pulmonary Disease (COPD) Overlap Syndrome.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- Elevated expression of NEU1 sialidase in idiopathic pulmonary fibrosis provokes pulmonary collagen deposition, lymphocytosis, and fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- IFN-γ directly controls IL-33 protein level through a STAT1- and LMP2-dependent mechanism.The Journal of biological chemistry · 2014Article
- Interleukin-33 potentiates bleomycin-induced lung injury.American journal of respiratory cell and molecular biology · 2013Article
- Cytokines in chronic respiratory diseases.F1000 biology reports · 2013Article
- Regulation of inflammation by interleukin-4: a review of "alternatives".Journal of leukocyte biology · 2012Review
- Full-length IL-33 promotes inflammation but not Th2 response in vivo in an ST2-independent fashion.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Natural production and functional effects of alternatively spliced interleukin-4 protein in asthma.Cytokine · 2012Article
- Comparative analysis of genome sequences of the Th2 cytokine region of rabbit (Oryctolagus cuniculus) with those of nine different species.Immunology and immunogenetics insights · 2011Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
IL-4δ2 is a natural splice variant of IL-4 that lacks the region encoded by the second exon. Numerous reports have suggested that the expression levels of IL-4δ2 change in various diseases, especially those with pulmonary involvement, but the in vivo effects of this splice variant have never been studied. Replication-deficient, AdV-mediated gene delivery of mIL-4δ2 to mouse lungs in vivo was used, and the effects compared with similar adenoviral delivery of mIL-4 or with infection with a noncoding NULL viral construct. Overexpression of IL-4δ2 or IL-4 caused pulmonary infiltration by T and B lymphocytes, whereas in contrast to IL-4, IL-4δ2 did not induce eosinophilia or goblet cell hyperplasia. Microarray analysis of global gene expression revealed that IL-4δ2 and IL-4 had differential effects on gene expression. These splice variants also differentially regulated pulmonary levels of the cytokines TNF-α, eotaxin, IL-1α, IFN-γ, and MCP-1, whereas both tended to increase total lung collagen modestly. Pulmonary infiltration by lymphocytes in response to overexpression of IL-4δ2 was attenuated but not abrogated completely by germline deficiency of IL-4Rα or STAT6, whereas deficiency of endogenous IL-4 had no effect. Thus, IL-4δ2 promotes lymphocytic inflammation in vivo (although differentially from IL-4, in part), and the effects of IL-4δ2 are not mediated by endogenous IL-4. Differential targeting of IL-4δ2 and IL-4 may therefore be considered in developing future therapeutic agents.
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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.