After incubation of macrophages with MVC for 24 h,

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After incubation of macrophages with MVC for 24 h, levels of M1 cytokines significantly increased, whereas those of M2 phenotype factors ARG1, TGF-β 1, and IL-10 decreased

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Exactly. Maraviroc, CCR5 blockade, LRM, all work to increase M1 activity while reducing M2 activity. M1 is the classical pathway. M2 is the alternative pathway. M1 is inflammatory and leads to macrophage killing. M2 is anti-inflammatory and leads to growth, healing, scarring, wound healing, remodeling. What does LRM do? LRM increases killing with nitric oxide which induces inflammation. What else does LRM do? It reduces the anti-inflammatory pathway. It reduces TGF-Beta, Transforming Growth Factor Beta which leads to healing. LRM reduces that. LRM reduces IL-10 which has an effect of reducing inflammation.

LRM CCR5 blockade promotes the immune system to do its job until the job is done. It's focus is not a reduction of inflammation. That is only a side effect. Its focus is restoration of health and it does that by getting the immune system to do its job.

From the other article you posted below:

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Cancer can “hijack” chemokine networks to support cancer progression. Substantial evidence points to major participation of CCL5 in the progression of liver diseases, especially HCC. Singh et al have observed a higher expression level of CCL5 in HCC tissues than in non-neoplastic liver tissues and found that CCR5–CCL5 interaction causes metastatic behavior of HCC cells.

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On the one hand, M2 macrophages can directly promote tumor cell growth by secreting cytokines such as IL-10. (Hijacked Immune System, the cancer has hijacked the immune system and has overtaken control of the chemokines to support the cancer's progression.) On the other hand, M2 macrophages can reduce the production of nitric oxide, (yes, there is no NO production in the M2 pathway) by blocking the inducible nitric oxide synthase pathway, thereby inhibiting tumor cell apoptosis.

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(exactly what you don't want to happen, but why is this happening?, because the M2 macrophage is in a zombie state, deluded by faulty cellular communication, controlled by the tumor.)

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In our study, macrophages receiving MVC tended to have M1-like properties with a decreased level of IL-10 in the supernatant.

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Yes, CCR5- blockade tends to ramp up the immune system, getting rid of faulty communication, so the immune system may properly operate to restore the healthy state with reduced inflammation. Since it resulted in reduced IL-10, which is reduced anti-inflammatory cytokine.

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In several cancer types, there exists upregulation of IL-10, the development of immune tolerance. IL-10 is expressed in gastric cancer metastases, and a positive correlation exists between serum IL-10 levels and progression of cancers .

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IL-10 is anti-inflammatory. Of course the cancer would want to recruit it to make the immune system "TOLERATE" the cancer. Therefore, in some cancers, there exists positive correlation between increased serum IL-10 levels and the progression of such cancers.

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In contrast, the expression of IL-10 is markedly increased in gastric cancers with lymph node metastasis. This unbalance between Th1/Th2 cytokines has been mechanistically linked to the high level of expression of RANTES and CCR5 in gastric cancers with lymph node metastasis, suggesting that RANTES/CCR5 axis might impair the regional immunity in these cancers

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Now, isn't this completely obvious? That when RANTES is involved, so is the misuse of IL-10. That the cancer exudes RANTES to overtake control of the macrophages and one of the cytokines it uses to its own advantage is IL-10. By increasing IL-10 by inducing a level of "TOLERANCE" for the cancer. To reduce the M1 pathway and instilling an anti-inflammatory effect surrounding the cancer, so it may proliferate.

RED = DELUSION

Bring on LRM and that all ends swiftly.