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The multiple and overlapping feedback loops are what maintains homeostasis across multiple biological systems.

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The entire point of targeting CCR5 in disease is that the increase in CCR5 is disrupting homeostasis. I am well aware of the feedback loops that exist with CCR5 which are based on the ligand activation. Let's take a look at CCL5 (RANTES), It also binds to CCR3 and CCR4. The
highest binding affinity is by far CCR5. CCR3 and CCR4 expression is a small fraction of CCR5 expression. In an over-reactive immune system you will see an increase in all CCR receptors but CCR3 and CCR4 are still a small increase compared to CCR5.

There is a feedback loop where CCL5 increases CCR5 expression and that increased expression further elevates CCL5 levels. Blockade of CCR5 breaks that loop at 700mg as can be seen in Patterson's paper - "CCR5 inhibition in critical COVID-19 patients decreases inflammatory cytokines, increases CD8 T-cells, and decreases SARS-CoV2 RNA in plasma by day 14".

Yet you see a dramatic increase in CCL5 levels at 700mg in the NASH poster.

As can be seen in a myriad of papers the increase in CCR5 receptor occupancy by any drug mirrors a decrease in chemokines.