Thanks for this. I appreciate knowing that, but this discusses cirrhosis when we were discussing NAFLD and NASH. As this is a progressive disease, CCR5 seems to be upregulated as the disease progresses, (in what I tend to think of as an exponential manner, which means, that the closer the patient gets to Cirrhosis, the more profound an increase in CCR5 would be appreciated), as the following from this study discusses:

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it is likely that RANTES and CCR5 are upregulated and promote fibrogenesis at later stages for the following reasons: (a) Our BMT model and
expression analysis as well as previous studies suggest that CCR5 mediates many of its profibrogenic effects in activated HSCs. These cells accumulate at later stages of fibrogenesis, and therefore CCR5 exerts its effects predominantly at late stages of fibrogenesis. Moreover, RANTES levels were higher at later stages of murine fibrogenesis than at early time points. (b) CCR5-deficient mice showed little inhibition of fibrogenesis at early time points, whereas CCR5 inhibition effectively decreased fibrogenesis at later time points. This hypothesis is further supported by the finding that CCR5 may play a role in the progression of chronic HCV infection.
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Thus, based on our results and genetic studies in patients with chronic hepatitis C, CCR5 antagonism by small-molecule inhibitors may represent a feasible and promising antifibrogenic approach.

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