I'll guess that this is old news to Ohm, but it's new to me, in spite of being from 2015. Very interesting article demonstrating that CCR5 is core to development of insulin resistance/type 2 diabetes.

https://www.tandfonline.com/doi/pdf/10.4161/adip.22420

CCR5: A novel player in the adipose tissue inflammation and insulin resistance?

Quote:

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First, expression of CCR5 and its ligands is significantly increased and is equal to that of CCR2 and its ligands in the white adipose tissue of obese mice, particularly in the macrophage fraction.

Second, fluorescence-activated cell sorter (FACS) analysis clearly demonstrates a robust increase in CCR5+ ATMs (Adipose Tissue Macrophages) in response to a HF diet even after normalizing for stromal vascular cell number and fat weight.

Third, and most important, Ccr5-/- mice are protected from insulin resistance, hepatic steatosis and diabetes induced by HF feeding. It is noteworthy that two distinct models, both Ccr5-/- mice and chimeric mice lacking CCR5 only in myeloid cells, are protected from HF diet- induced hyperinsulinemia and glucose intolerance through, at least in part, a reduction in ATM accumulation. Finally, it is interesting that an M2-dominant shift in ATM is induced in obese Ccr5-/- mice.

Therefore, we conclude that deficiency of CCR5 causes an M2-dominant phenotypic shift in ATMs, which contributes to the attenuation of obesity-induced insulin resistance.

Additionally, a bone marrow transplantation study [The effect which would be achieved through Leronlimab administration] revealed that lack of CCR5 expression in macrophages alone was sufficient to protect mice from the HF diet-induced insulin resistance

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I know diabetes is on the Ohm master list, but it is nonetheless compelling to have the mechanism by which leronlimab can overcome insulin resistance described exactly.