I don't think Actemra works "against" IL-6. From what I have read, it binds with the receptors of IL-6. These IL-6 receptors (IL-6R) are everywhere in the body. When the cytokine IL-6 binds to these receptors it causes a pro-inflammatory response. This triggers a cascade of immune related responses throughout the body which in turn causes unregulated "systemic inflammation."

Inflammation isn't inherently bad so long as it is regulated. One of the primary functions of cortisol is to "regulate" inflammation. When we take prednisone it is in an attempt to help the immune system regulate inflammation when the immune system goes haywire for some reason. The extra cortisol we take in the form of prednisone decreases the amount of inflammation to a more manageable level.

When Actemra binds to IL-6 receptors, the cytokine IL-6 has nowhere to go except that it stays in the bloodstream and IL-6 blood levels skyrocket. The body then down regulates the amount of the cytokine IL-6 in the bloodstream. Somehow IL-6 levels return to normal levels. It isn't clear to me why this happens except that the body likes to be in a state of equilibrium.

This is all from an interesting hypothesis that took me a while to fully understand. It is called the "bathtub theory" for the mechanism of action of Actemra for RA.

It is all a theory so take it for what it is worth. The diagram in the link below shows a red Y-shaped thing binding to an IL-6 receptor. It took me forever to figure out what that was.
https://www.researchgate.net/figure/Mechanism-of-action-of-tocilizumab-in-RA-bathtub-theory-Notes-The-mechanism-of_fig2_221967570
It is as clear as mud.