IL-23p19 in osteoarthritic pain and disease
Kevin M-C Lee1, Tanya Lupancu1, Adrian A Achuthan1
1Department of Medicine, Royal Melbourne Hospital, The University of Melbourne, Parkville, Victoria 3050, Australia.
Osteoarthritis and Cartilage
|June 6, 2024
Summary
Interleukin-23 p19 subunit (IL-23p19) drives osteoarthritis (OA) pain and disease progression in mouse models. Targeting IL-23 may offer new treatments for OA pain and joint damage.
Area of Science:
- Immunology
- Rheumatology
- Pain Medicine
Background:
- Inflammation is a hallmark of osteoarthritis (OA), yet interleukin-23 (IL-23) is not a typical therapeutic target.
- Previous research established the role of IL-23 p19 subunit (IL-23p19) in arthritic pain and disease.
Purpose of the Study:
- To investigate the role of IL-23p19 in osteoarthritis (OA) pain and disease.
- To explore IL-23p19 as a potential therapeutic target for OA.
Main Methods:
- Utilized two mouse models of OA: collagenase-induced and monosodium iodoacetate-induced OA.
- Assessed pain-like behavior and arthritis severity (histology) in IL-23p19 gene-deficient mice.
- Correlated IL-23A gene expression with Oxford knee score (OKS) in human OA patient synovial tissues.
Main Results:
- IL-23p19 deficiency attenuated pain-like behavior, cartilage damage, and osteophyte formation in experimental OA.
- IL-23A gene expression in OA synovial tissues negatively correlated with Oxford knee score (OKS).
Conclusions:
- IL-23p19 is essential for OA pain and disease development.
- Targeting IL-23 presents a promising therapeutic strategy for managing OA pain and progression.
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