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What was it exactly that Dr. Maddon & CytoDyn actually claimed for years? That LL is a blockade of CCR5?

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From December 2020 -

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Leronlimab (PRO 140) only blocks the precise site on CCR5 that HIV needs to enter the cell without interfering with the normal functions of CCR5.

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At the same time they claimed this, which if the previous statement was true then it would have no effect on cancer or any other disease but HIV.

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CCR5 for Cancer

Developing CCR5 Technology in Cancer Indications

Based on the work of of a leading oncologist and researcher who has played an instrumental role in identifying the role of CCR5 in cancer indications, we continue to develop CCR5 technology and have obtained promising results from various pre-clinical studies.

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That capacity to inhibit these ligands only at CCR5, but having no inhibition at the other receptors does not inhibit the adaptive immune response, but does inhibit the inflammatory cascade.

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The inflammatory cascade is a result of an immune response. Leronlimab inhibits both the immune response and the inflammatory cascade. In both cases it is inhibiting an over-reactive response and bringing both back to normal levels.

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I'm not sure I understand your last paragraph. Why are the "other" chemokines elevated? Are you saying that in a disease process, CCR5 is elevated and "ALL" the associated ligands, CCL2-5, and others are also elevated in turn? I don't see why this elevation of both the receptors and all the ligands brings it to a normal state.

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The CCR receptors and chemokines increase greatly due to any insult to the body, whether it's pathogen, physical injury or poisons. The CCR receptors are very few in number compared to CCR5 and usually have less binding affinity to CCR5 bindable chemokines. With CCR5 blocked the other now more numerous receptors and the chemokines that have nowhere else to bind except the other CCR receptors may equal what a normal immune response would be.