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He seems to feel that statins are especially good at dealing with fractalkine receptors on the endothelial layer of blood vessels. These are the receptors that can anchor non-classical monocyte macrophages to the endothelium, which is not so good, causing inflammation, especially in the blood vessels of the brain.

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How statins effect the fractalkine receptor (CX3CR1) is by downregulating it's ligand CX3CL1. CCR5 blockade also downregulates CX3CL1 via NF-kB and TNF-a downregulation and it's on the regulator list.

Statins reduce adhesion to the endothelial layer by reduction of ICAM-1 (intercellular adhesion molecule-1) via disruption of the IFN-y pathway. With CCR5 blockade downregulating IFN-y then it comes as no surprise that CCR5 blockade also downregulates ICAM-1. But CCR5 blockade has another trick up it's sleeve. ICAM-1 binds to LFA-1 (lymphocyte function–associated antigen-1) which are present in those macrophages that are binding to the endothelium. CCR5 blockade also downregulates LFA-1.

Patterson may be using statins because of maraviroc's lower efficacy compared to leronlimab. Possibly statins could even give a little boost to leronlimab. But from our own trial we have a decent idea of what leronlimab can do on it's own.