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Chemokines exist in the body at low levels even if an inflammatory response doesn't exist or even when an immune response isn't needed. They also bind to CCR5 under those conditions. When leronlimab binds to CCR5 those chemokines remain unattached and spur the formation of new CCR5 receptors.

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If it is not by the cells of the immune system, (CD4, CD8, macrophages, neutrophils, dendrites, natural killer cells, eosinophils, basophils, t helper, t regulators), that chemokines are manufactured, then by what means are chemokines produced?

If the level of chemokine in the serum was sufficient, then why were there insufficient quantites of CCR5 on the surface of CD4 cells in these LH patients with supposedly dead immune systems? Why did it require the binding of LL to CCR5 to induce the cell to manufacture more CCR5 to be expressed on their surface? If the inflammatory chemokine interferon gamma was present, should it not have motivated the CD4 cell to wake the hell up, express more CCR5 and start manufacturing antibodies against the spike proteins?

The only thing that I thought you suggested was that you stated that the chemokines induced CCR5 manufacture and subsequent expression. I liked that idea and went with it. I think you're right in that, but I apparently, in your estimation, I was wrong to think you were right.

This last statement:

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You also seem to be unaware that cells have life cycles and leronlimab can bind to new cells as they form and the older ones that are already bound with chemokines will die off.

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is untrue and not applicable.
If we have to wait for the immune system to regenerate before LL works, this investment is worthless.