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This matters because PD-L1 expression is required for many patients to benefit from checkpoint inhibitor drugs (like Keytruda).

???? What This Means:
PD-L1 is like a molecular “flag” that makes tumors visible to the immune system — high PD-L1 = better chance ICIs will work.

Most triple-negative breast cancers are “cold,” meaning they don’t show this flag, so ICIs usually don’t work.

But leronlimab induced PD-L1 in these patients — potentially converting cold tumors into hot tumors.

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A bit backwards. Bound PD-L1 puts a "do not kill" sign on tumor cells when binding to PD-1 on immune cells so that killer cells ignore the tumor. It makes it invisible to the immune system. PD-1 blockers like Keytruda block PD-L1 from binding to PD-1 so they become visible to the immune system.

An increase in PD-1/PD-L1 is a response to an increase in immune system activation and numerous killer cells around the tumor. What can specifically drive upregulation of PD-1/PD-L1 is CCL5 induced upregulation of the JAK/STAT3 pathway, TGF-b and IFN-y (all downregulated by leronlimab).

It could be the much stronger binding efficacy of leronlimab vs. maraviroc is increasing immune response to a level that the downregulation of chemokines is not enough to deter the upregulation of PD-L1. It could also be that leronlimab is increasing PD-L1 but decreasing or not increasing at the same rate PD-1 leaving unbound PD-L1. It would be interesting to know whether the PD-L1 measured was unbound PD-L1 or whether they measured unbound PD-1 levels.