Innovation Pharmaceuticals Inc (IPIX)

[georgejjl]

Because Prurisol potently inhibits IL-20, then Prurisol will be safe and effective as a treatment for rheumatoid arthritis!!!

The IL-20 Cytokine Family in Rheumatoid Arthritis and Spondyloarthritis.
Kragstrup TW1,2, Andersen T1, Heftdal LD1, Hvid M1,3, Gerwien J4, Sivakumar P5, Taylor PC6, Senolt L7, Deleuran B1,2,3.
Author information
1
Department of Biomedicine, Aarhus University, Aarhus, Denmark.
2
Department of Rheumatology, Aarhus University Hospital, Aarhus, Denmark.
3
Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
4
Eli Lilly, Herlev, Denmark.
5
Immuno Oncology Translational Development, Celgene Corportation, Seattle, WA, United States.
6
Nuffield Department of Orthopedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, United Kingdom.
7
Institute of Rheumatology and Department of Rheumatology, First Faculty of Medicine, Charles University, Prague, Czechia.
Abstract
This review describes the IL-20 family of cytokines in rheumatoid arthritis (RA) and spondyloartrhitits (SpA) including psoriatic arthritis. The IL-20 receptor (R) cytokines IL-19, IL-20, and IL-24 are produced in both the peripheral blood and the synovial joint and are induced by Toll-like receptor ligands and autoantibody-associated immune complexes in monocytes. IL-19 seems to have anti-inflammatory functions in arthritis. In contrast, IL-20 and IL-24 increase the production of proinflammatory molecules such as monocyte chemoattractant protein 1 and are associated with bone degradation and radiographic progression. IL-22 is also associated with progression of bone erosions. This suggests that the IL-22RA1 subunit shared by IL-20, IL-22, and IL-24 is important for bone homeostasis. In line with this, the IL-22RA1 has been found on preosteoclasts in early RA. IL-26 is produced in high amounts by myofibroblasts and IL-26 stimulation of monocytes is an important inducer of Th17 cells in RA. This indicates a role for IL-26 as an important factor in the interactions between resident synovial cells and infiltrating leukocytes. Clinical trials that investigate inhibitors of IL-20 (fletikumab) and IL-22 (fezakinumab) in psoriasis and RA have been terminated. Instead, it seems that the strategy for modulating the IL-20 cytokine family should take the overlap in cellular sources and effector mechanisms into account. The redundancy encourages inhibition of more than one cytokine or one of the shared receptors. All IL-20 family members utilize the Janus kinase signaling pathway and are therefore potentially inhibited by drugs targeting these enzymes. Effects and adverse effects in ongoing clinical trials with inhibitors of IL-22 and the IL-22RA1 subunit and recombinant IL-22 fusion proteins will possibly provide important information about the IL-20 subfamily of cytokines in the future.

https://www.ncbi.nlm.nih.gov/pubmed/30319661

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Good luck and GOD bless,

George