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Published on: November 26, 2015
Basic and Translational Science: A Report from the GRAPPA 2016 Annual Meeting
James G Krueger1,2, Bruce Kirkham1,2, Christopher T Ritchlin3,4
1From Clinical Investigation, The Rockefeller University, New York; Division of Allergy, Immunology, and Rheumatology, University of Rochester Medical Center, Rochester, New York, USA; Guy's and St. Thomas' UK National Health Service (NHS) Foundation Trust; King's College London, London, UK.
New understanding of innate immunity reveals the interleukin (IL)-23-IL-17 axis is key to psoriasis and psoriatic arthritis inflammation. This knowledge drives advancements in effective treatments for these conditions.
Area of Science:
- Immunology
- Dermatology
- Rheumatology
Background:
- Psoriasis and psoriatic arthritis (PsA) treatments are advancing due to a better grasp of inflammatory processes.
- Innate immunity and specific cytokines, particularly within the IL-23-IL-17 axis, are recognized as crucial in psoriatic disease pathogenesis.
Purpose of the Study:
- To summarize recent scientific discussions regarding the IL-17-related pathways.
- To explore the connection between IL-17 pathways and the development of psoriasis and PsA.
Main Methods:
- Literature review of recent advancements in understanding psoriasis and PsA.
- Analysis of the role of innate immunity and cytokine involvement, specifically the IL-23-IL-17 axis.
Main Results:
- Improved understanding of cell subsets and mediators driving inflammation and tissue damage in psoriasis and PsA.
- Identification of the IL-23-IL-17 axis as a central pathway in psoriatic plaque and joint inflammation.
Conclusions:
- The IL-23-IL-17 axis is a critical mediator in the immunopathogenesis of psoriasis and PsA.
- Advances in understanding these pathways are paving the way for more effective therapeutic strategies.
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