"Actemra inhibits IL-6, but there are other substances that cause the inflammation from PMR and GCA,"
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True ... but cytokines aren't separate and independent inflammation pathways. The cytokines are more like a network of things that talk to each other and influence each other. I can barely understand what IL-6 does when my rheumatologist goes on and on about "crosstalk" and "upstream and downstream regulation" of things. Cortisol might be the conductor of the orchestra that keeps everything in balance and maintains the harmony.

My rheumatologist says 1L-17 inhibition might be another option for me and has suggested Cosentyx. It might work for both PMR and spondyloarthritis.
https://www.drugs.com/cosentyx.html#:~:text=Cosentyx%20FDA%20approval%20was%20received,immune%20system%20to%20fight%20infections.
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I think IL-17 inhibition is being studied for PMR but medical research is painstakingly slow. There will be plenty of time to do painstakingly slow tapers off Prednisone.

Thank God they are actively seeking alternatives to Prednisone.
https://www.healio.com/news/rheumatology/20250220/tsunami-of-effortbrings-biologics-to-the-forefront-in-giant-cell-arteritis-pmr#:~:text='Really%20Exciting'%20Data%20in%20IL,in%20both%20PMR%20and%20GCA.%E2%80%9D
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Janus kinase (JAK) inhibitors such as upadacitinib (Rinvoq) are also being evaluated for both PMR and GCA.

For now, I'm content to stay on Actemra.

Thanks for your comment. Do t know whether I read this or it seems sensible but have wondered if PMR patients vary on the specific immune pathways that trigger the symptoms. Based on Kevzara response, IL-16 is certainly a major pathway for my PMR but presence of other autoimmune disorders suggests other pathways might take a supporting role. Appreciate your comments.