Many thanks to you ohm, for providing the link to

Many thanks to you ohm, for providing the link to that study.

More evidence that in bold which shows RANTES helping the Tumor survive:

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Interestingly, tumor cells also included a relatively high proportion of CCR5+ cells (figure 5C). We stimulated the isolated BAP1-mutant renal tumor cells with CCR5 ligands in vitro with addition of maraviroc. Subsequent analysis revealed CCL5 could significantly enhanced PD-L1 expression by tumor cells, followed by CCL3 and CCL8. However, this effect was reversed after blocking CCR5 (figure 5D). Moreover, blockade of CCR5 caused PD-L1 expression to decrease without addition of exogenous chemokines.

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and

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Similarly, Zhang et al found that colon cancer cells recruited CCR5+ Tregs to local tumors by secreting CCL5, which in turn suppressed the cytotoxicity of CD8+ T cells and mediated immune evasion.19 28

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Previous studies have reported the high expression of CCR5 and its ligand CCL5 in basal and HER-2 breast cancer, revealing that CCR5 plays a crucial role in cancer progression.11 23 Taken together, these results suggested that targeting CCR5 might serve as a novel strategy in cancer treatment.

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I bet when the MD Anderson study is done, that they will determine that the monoclonal antibody they're studying in combo with the check point inhibitor it is paired with, in addition to performing it's CCR5 blockade functionality flawlessly, functions as a better check point inhibitor than the check point inhibitor it is being paired with.

On the surface of the T-Cells, the proximity of CCR5 to CD4 is also very close to the check point PD-1 is very close to CD4 which makes it also close to CCR5. Therefore, when LL binds to CCR5, it physically interferes and inhibits the binding of PD-1 to the PD-L1 ligand on the tumor cell, (thereby also acting as a PD-1 check point inhibitor) and when the T-Cell examines the tumor for friend or foe, when the check point is not matched with the tumor's ligand, the tumor cell self destructs due to activation of the "Programmed Cell Death" PD of the tumor cell. Maraviroc, being a pyrimidine small-molecule CCR5 inhibitor, much smaller than LL is not big enough to interfere with the PD-1 check point and does not perform PD-1 inhibition as well. Gotta have LL.