Nobody really knows how IL-6 "inhibitors" work. There was one theory that fascinated me. The production of IL-6 isn't actually stopped according to the theory. The overproduction of IL-6 is "reset" to normal levels.

Google the "bathtub theory of IL-6 blockade."

The following diagram illustrates the mechanism:

The red "Y' shaped thing is a molecule of tocilizumab that binds with IL-6 receptors. Don't overlook the small "drain" at the bottom which says IL-6 catabolism which is how IL-6 is normally eliminated from the body.
https://www.researchgate.net/figure/Mechanism-of-action-of-tocilizumab-in-RA-bathtub-theory_fig2_221967570
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In the context of rheumatoid arthritis (RA) artificial intelligence says the following but it is still a theory.

"In RA, the "faucet" (immune cells) is constantly open, producing excessive IL-6, and the "drain" (clearance mechanisms) can't keep up.

This leads to an overflow of IL-6 into the "drain" (IL-6 receptors), driving inflammation and joint damage.

Tocilizumab, an IL-6R blocking antibody, "blocks the drain", preventing IL-6 from binding to its receptors and initiating inflammatory signaling.

However, tocilizumab does not inhibit IL-6 production itself. Therefore, as the receptors are blocked, the unbound IL-6 accumulates in the serum, leading to a temporary increase in circulating IL-6 levels.

Over time, tocilizumab helps normalize the IL-6 levels by reducing the underlying immune activation and inflammation, effectively "closing the faucet" and allowing serum IL-6 levels to decrease."