I was going to leave that alone because that paper was a bit of a mess. But I received an email with a link to an article that made me decide to look at the Kennedy paper which is what they cited as to the type of mice they used.
https://www.sciencedaily.com/releases/2020/04...112520.htm
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3798705/
The problem with the paper linked in the earlier post and Kennedy's paper is the use of CCR5 null mice. In the linked paper there is also the problem of the CCR5 antagonist having to be small molecule like maraviroc and using the metCCL5 antagonist.

In Kennedy's paper it's shown the CCR5 null mice increase CD4+ cell production adding to the inflammation and glucose intolerance. We know leronlimab's partial CCR5 blockade reduces CD4+, the accompanying inflammation and would reduce the glucose intolerance.

Quote:

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In addition, HF feeding caused a twofold increase in CD4+ T cells in the AT of CCR5−/− compared with WT mice.

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Using a CCL5 antagonist is not relevant to leronlimab because the pathway they are talking about in the hypothalamus is not CCR5 dependent.

Quote:

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One of CCL5/RANTES’s receptors, GPR75 (G-protein receptor 75), on the pancreatic β-cell membrane is involved with stimulating insulin secretion and improves glucose homeostasis in both lean mice and ob/ob insulin resistant mice

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https://www.nature.com/articles/srep37659