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Interleukin-23 Involved in Fibrotic Autoimmune Diseases: New Discoveries.
Margherita Sisto1, Sabrina Lisi1
1Department of Translational Biomedicine and Neuroscience (DiBraiN), Section of Human Anatomy and Histology, University of Bari "Aldo Moro", 70123 Bari, Italy.
Journal of Clinical Medicine
|September 9, 2023
Summary
Interleukin-23 (IL-23) drives inflammation and fibrosis in autoimmune diseases. Targeting IL-23 may offer new treatments for these fibrotic conditions.
Area of Science:
- Immunology
- Pathology
- Rheumatology
Background:
- Interleukin-23 (IL-23) is a key pro-inflammatory cytokine.
- IL-23 promotes T helper type 17 (Th17) cell differentiation and proliferation via IL-17 and IL-22.
- Emerging evidence links IL-23 to fibrosis in chronic inflammatory autoimmune diseases.
Purpose of the Study:
- To review the biological characteristics of IL-23.
- To summarize current research on IL-23's role in fibrotic autoimmune conditions.
- To provide a foundation for clinical targeting and drug development.
Main Methods:
- Literature review of biological features of IL-23.
- Synthesis of recent research on IL-23 in fibrotic autoimmune diseases.
Main Results:
- IL-23 is a central mediator of pro-inflammatory cytokines IL-17 and IL-22.
- IL-23 plays a significant role in the pathogenesis of fibrosis in autoimmune diseases.
- Understanding IL-23's fibrotic effects is crucial for therapeutic strategies.
Conclusions:
- IL-23 is implicated in the fibrotic processes of autoimmune diseases.
- Targeting IL-23 presents a promising avenue for treating fibrotic autoimmune conditions.
- Further research into IL-23's pro-fibrotic mechanisms can guide clinical interventions.
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