Related Experiment Video
Updated: Mar 24, 2026
07:23
Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome
Published on: June 15, 2016
9.0K
Treating psoriasis by targeting its susceptibility gene Rel
Tingting Fan1, Shaowen Wang1, Linjiang Yu1
1Shenzhen Laboratory of Fully Human Antibody Engineering, Institute of Biomedicine and Biotechnology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, People's Republic of China.
Clinical Immunology (Orlando, Fla.)
|March 20, 2016
Summary
Targeting the c-Rel mRNA with siRNA prevented and treated psoriasis in mice. This approach inhibited key inflammatory cytokines like IL-23, offering a new therapeutic strategy for this chronic skin condition.
Area of Science:
- Dermatology
- Immunology
- Molecular Biology
Background:
- Psoriasis is a chronic inflammatory skin disease.
- The Rel gene (a member of the NF-κB family) is implicated as a risk factor for psoriasis.
- Targeting the c-Rel mRNA presents a potential therapeutic avenue.
Purpose of the Study:
- To investigate the prevention and treatment of psoriasis by targeting the c-Rel mRNA.
- To evaluate the efficacy of c-Rel specific siRNA (siRel) in a mouse model of psoriasis.
Main Methods:
- Utilized chemically-modified c-Rel specific siRNA (siRel) encapsulated in PEG-PLL-PLLeu micelles.
- Assessed c-Rel gene knockdown and its effect on downstream targets like IL-23.
- Employed an imiquimod (IMQ)-induced mouse model to study psoriasis development and treatment.
Main Results:
- Successfully achieved knockdown of c-Rel expression using siRel.
- Demonstrated significant inhibition of IL-23 cytokine expression, a key driver of IL-17-producing T cells.
- Showed that siRel treatment prevented and ameliorated IMQ-induced psoriasis in mice.
- Observed down-regulation of multiple inflammatory cytokines following siRel treatment.
Conclusions:
- Targeting the susceptibility gene Rel via its mRNA transcript is a viable strategy for psoriasis treatment and prevention.
- siRel effectively inhibits key inflammatory pathways involved in psoriasis pathogenesis.
- This study provides a foundation for developing novel RNA-based therapies for psoriasis.
Related Concept Videos
01:20The JAK-STAT Signaling Pathway
13.8K
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...
13.8K
01:24T Cell Types and Functions
3.2K
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
3.2K
02:26NF-κB-dependent Signaling Pathway
10.3K
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
NF-κB-dependent Signaling Mechanism
The...
10.3K
01:16TGF - β Signaling Pathway
10.9K
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
10.9K
01:29Pharmacogenomics: Identification of New Drug Targets
76
Advances in genomics have profoundly influenced drug discovery by increasing both the speed and accuracy of pharmaceutical development. Pharmacogenomics, which examines how genetic variation influences drug response, facilitates the identification of novel therapeutic targets and enables patient stratification for personalized treatment. These strategies contribute to improved drug efficacy, minimized adverse effects, and more efficient clinical trial design.Mapping genetic differences...
76
01:11Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
66
Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
66