I don't think Actemra destroys the IL-6 receptor. The receptors are still functioning except the cytokine IL-6 has to compete with the Actemra molecule. To the extent that Actemra doesn't trigger a pro-inflammatory response like the cytokine IL-6 does, I would guess this would reign in the systemic inflammation. Pure speculation on my part.

From my personal experience with stopping Actemra --- my symptoms gradually returned within a couple of months. My rheumatologist said what I reported to him was consistent with what other patients have reported. I assume the IL-6 inflammatory pathway is still functioning after Actemra is stopped.

Does this answer your question?

I have read about cases where patients have a deficiency of IL-6 receptors. This seems to predispose them to immunodeficiency so they are infection prone.
https://rupress.org/jem/article/216/9/1986/120703/Loss-of-the-interleukin-6-receptor-causes
I haven't ever read anything that said Actemra can cause this.

If you are interested, the following link is understandable and talks about the evolution of IL-6 targeted treatments.
https://www.nature.com/articles/s41584-020-0419-z