ArticleMolecular therapy : the journal of the American Society of Gene Therapy2013
IL10 released by a new inflammation-regulated lentiviral system efficiently attenuates zymosan-induced arthritis.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
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- Cyclooxygenase 2 Effector Genes as Potential Inflammation-Related Biomarkers for Colorectal Cancer Circulating Tumor Cells Detection by Liquid Biopsy.Frontiers in pharmacology · 2021Article
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- Biochanin A attenuates zymosan-induced arthritis in mice similarly to 17-β estradiol: an alternative to hormone replacement therapy?Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Article
- CCR7 as a novel therapeutic target in t-cell PROLYMPHOCYTIC leukemia.Biomarker research · 2020Article
- IL-7R is essential for leukemia-initiating cell activity of T-cell acute lymphoblastic leukemia.Blood · 2019Article
- Intratumoral expression using a NFkB-based promoter enhances IL12 antitumor efficacy.Cancer gene therapy · 2019Article
- Clonal dynamics in osteosarcoma defined by RGB marking.Nature communications · 2018Article
- The NOTCH1/CD44 axis drives pathogenesis in a T cell acute lymphoblastic leukemia model.The Journal of clinical investigation · 2018Article
- Intra-articular drug delivery systems for joint diseases.Current opinion in pharmacology · 2018Review
- Genome Engineering for Personalized Arthritis Therapeutics.Trends in molecular medicine · 2017Review
- Genome Engineering of Stem Cells for Autonomously Regulated, Closed-Loop Delivery of Biologic Drugs.Stem cell reports · 2017Article
- Suppression of the inflammatory response by disease-inducible interleukin-10 gene therapy in a three-dimensional micromass model of the human synovial membrane.Arthritis research & therapy · 2016Article
- Assembly PCR synthesis of optimally designed, compact, multi-responsive promoters suited to gene therapy application.Scientific reports · 2016Article
- Efficient expression of bioactive murine IL12 as a self-processing P2A polypeptide driven by inflammation-regulated promoters in tumor cell lines.Cancer gene therapy · 2015Article
- Patient-derived olfactory mucosa for study of the non-neuronal contribution to amyotrophic lateral sclerosis pathology.Journal of cellular and molecular medicine · 2015Article
- GAPDH enhances the aggressiveness and the vascularization of non-Hodgkin's B lymphomas via NF-κB-dependent induction of HIF-1α.Leukemia · 2015Article
- Specific calcineurin targeting in macrophages confers resistance to inflammation via MKP-1 and p38.The EMBO journal · 2014Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Administration of anti-inflammatory cytokines is a common therapeutic strategy in chronic inflammatory diseases. Gene therapy is an efficient method for delivering therapeutic molecules to target cells. Expression of the cell adhesion molecule E-selectin (ESEL), which is expressed in the early stages of inflammation, is controlled by proinflammatory cytokines, making its promoter a good candidate for the design of inflammation-regulated gene therapy vectors. This study describes an ESEL promoter (ESELp)-based lentiviral vector (LV) that drives localized transgene expression during inflammation. Mouse matrigel plug assays with ESELp-transduced endothelial cells showed that systemic lipopolysaccharide (LPS) administration selectively induces ESELp-controlled luciferase expression in vivo. Inflammation-specific induction was confirmed in a mouse model of arthritis, showing that this LV is repeatedly induced early in acute inflammation episodes and is downregulated during remission. Moreover, the local acute inflammatory response in this animal model was efficiently blocked by expression of the anti-inflammatory cytokine interleukin-10 (IL10) driven by our LV system. This inflammation-regulated expression system has potential application in the design of new strategies for the local treatment of chronic inflammatory diseases such as cardiovascular and autoimmune diseases.
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