I have asked my rheumatologist about targeting a cytokine and blocking it instead of treating a diagnosis. The explanation was that cytokines form a "communication network" complete with upstream and downstream regulation along with "crosstalk." He said there is no such thing as a single inflammation pathway that can be isolated and treated. He said it was more like turning down the cytokine that is the loudest versus blocking it completely. These pathways are interconnected and influence each other, making it challenging to isolate and treat a single pathway without affecting the others. It was a complicated explanation.

My rheumatologist was very animated about the topic but I didn't understand much of anything that he said. He also mentioned that Rinvoq might work because of how it regulates IL-6.

According to artificial intelligence --- "Rinvoq (upadacitinib) works by targeting the Janus kinase (JAK) pathway, which is involved in signaling for various inflammatory processes, including those influenced by cytokines like IL-6."
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I was absolutely devastated by the flare of uveitis that I had almost as soon as I was able to taper off Prednisone. It is after my cortisol level improved. My ophthalmologist insisted on starting Humira (TNF-inhibitor) instead of Actemra.

Humira along with 60 mg of Prednisone worked for the flare of uveitis. Unfortunately, I was stuck on 15 mg of Prednisone when I tried to taper off Prednisone again. My rheumatologist eventually conceded that it would be impossible to treat all my autoimmune conditions with a single medication. Since I couldn't be on two biologics, he told me to pick the biologic that worked the best so I chose to restart Actemra.