Related Experiment Video
Updated: Dec 9, 2025
10:30
Visualization of IL-22-expressing Lymphocytes Using Reporter Mice
Published on: January 25, 2017
9.2K
Decoding IL-23 Signaling Cascade for New Therapeutic Opportunities
Gloria Pastor-Fernández1, Isabel R Mariblanca1, María N Navarro1
1Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas and Universidad Autónoma de Madrid (CSIC/UAM), 28049 Madrid, Spain.
Cells
|September 10, 2020
Summary
Interleukin 23 (IL-23) drives chronic inflammatory diseases. This review explores IL-23 signaling pathways, highlighting new therapeutic targets beyond current antibody treatments for conditions like psoriasis and rheumatoid arthritis.
Area of Science:
- Immunology
- Molecular Biology
- Pharmacology
Background:
- Interleukin 23 (IL-23) is a critical pro-inflammatory cytokine implicated in chronic inflammatory diseases including psoriasis, inflammatory bowel diseases, multiple sclerosis, and rheumatoid arthritis.
- Excessive IL-23 signaling promotes inflammatory mediators like IL-17, IL-22, GM-CSF, and TNFα, primarily via Th17 and Tγδ17 cells.
Purpose of the Study:
- To review current knowledge on proximal signaling events triggered by IL-23.
- To identify novel therapeutic intervention opportunities for IL-23-mediated pathologies.
Main Methods:
- Literature review of IL-23 signaling pathways.
- Analysis of existing and potential therapeutic strategies targeting IL-23.
Main Results:
- Monoclonal antibodies targeting IL-23 and IL-17 show efficacy but have limitations, with some patients exhibiting non-response or partial response.
- Alternative strategies, such as small molecule inhibitors and interfering peptides targeting intracellular signaling cascades, remain underexplored for IL-23-mediated diseases.
Conclusions:
- Combination therapies may be necessary for effective management of inflammatory diseases.
- Further research into intracellular signaling inhibition offers promising avenues for novel IL-23-targeted therapies.
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