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Leron occupies the CCR5 receptor. It is a CCR5 antagonist, but doesn't destroy them, allowing immune cells to remain functional. So I would assume the CCR5 count would remain the same.

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Binding of CCR5 by leronlimab keeps those receptors on the surface rather than retreating back into the cell. But there's a feedback loop between cytokines and CCR5 that will increase both and leronlimab disrupts that which should lower counts of both. HIV is an exception since HIV leads to a major downregulation of CD4/CCR5 cells and with treatment by leronlimab they rebound to a normal level restoring immune function.

CCR5 bound by leronlimab would have no immune capability since it binds to the CCR5's n-terminus blocking CCL cytokines from binding. But that slack would be taken up by the other CCR receptors allowing immune functionality.