That treatment boosts Tregs, leronlimab downregulates Tregs. Leronlimab also downregulates IL-2 and GM-CSF. If you use that treatment for inflammatory diseases you better hope to hell you never get cancer because Tregs and that type of anti-inflammatory environment protect tumors. Too much of a tilt to an anti-inflammatory state can also weaken immune response.

Leronlimab induces an M2 pro-inflammatory macrophage state. My theory - But blocks the ligands and downregulates the chemokines that can most make use of those macrophages. Leaving it up to the weaker CCR receptors to pick up the slack leading to a state of homeostasis in immune response where CD8+ T-cells and especially NKT cells can do their job. That homeostasis also leads to a normal rather than an overactive inflammatory response.