The only one he tested was CCL5 (RANTES) and ler

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The only one he tested was CCL5 (RANTES) and leronlimab blocked that.

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Therefore to the CCR5 receptor, LL competitively out binds RANTES & HIV.

And when LL does out bind RANTES, then what happens? The immune system goes to work as it should. Inflammation goes down because Disease goes away and healing begins. The immune system, when operating properly, eradicates disease and restores health. Therefore, the immune system reduces inflammation when it works properly. That is the overall end goal.

With higher CCR5 expression in the haplotype, 700mg LL did wonders both on PDFF as well as cT1. Why? Because LL allowed normal functionality of the immune system in and around the hepatocytes reducing lipogenesis, reducing cell apoptosis, and reducing the release of more chemokines to attract more cytokines which would have lead to more natural killer cells to the liver which would have led to an increase in scar tissue. All of that was reduced because LL restores proper immune functioning which restores proper hepatocyte functioning which reduces steatosis and scar tissue formation.

In Long Haulers, patients have zero immune system. All they have are an over worked, over burdened, fatigued immune system which do not eradicate spike proteins even if you put them smack dab infront of a Natural KIller Cell even if the spike protein was handed to it on a silver antigen presention platter.

No, it would shrug it off and leave it be! Why? CCL5 clogged up all the CCR5 receptors on the Tregs and caused all the Tregs to be active in REGULATING or SUPPRESSING the immune system in Long Haulers.

Why are the Tregs confused about what is self and what is foreign? Why can the T regs not recognize spike protein from self when they were trained in the thymus about exactly what is self and what is not self? Why Not? Because the T regs CCR5 receptors were fully bound by CCL5 RANTES and then internalized the CCR5 receptors thereby reducing their cell surface expression which was found in the Long Haulers trial. The mass quantity of RANTES made the T regs stupid traitors.

That means when ever there was a NKC or a Macrophage or a Dendrite cell presenting a spike protein asking the T reg if it should have the spike protein for dinner, the T reg says, "No, put that back; you are never to eat that"

Also, to add insult to injury, the Innate Immune system puts out the fuel for both the T regs and the Adaptive Arm, which is Interleukin 2. Without IL2, T regs are done and so is the adaptive arm. But there are lots of IL2 receptors on T regs. So when T regs are operating, they consume all the Interleukin 2 and the adaptive arm gets none. So the adaptive arm falls asleep by the wayside. The adaptive arm has no energy, no will to live, no get up and go without Interleukin 2, which is exactly what the T regs want, a SUPPRESSED IMMUNE SYSTEM. This is Long Haulers.

Bring on Leronlimab. All the CCL5 RANTES are immediately dislodged from the CCR5 receptors on the Tregs. Tregs are immediately awakened from their trance. Immediately, aware of their recent zombie phase, now, no longer confounded by the harming effect of CCL5 RANTES. All of a sudden, the T regs can tell what is self from what is foreign. The T regs remove their REGULATORY / SUPPRESSIVE control on the NKCs, Dendrites and CD8 Cytotoxic Killer Cells causing the Adaptive Arm of the Immune system to immediately return back to attack mode destroy the spike protein leading to health. The Immune system returns back and does what it was designed to do.

Why does RANTES confound the T reg, where it attaches at the same N terminus on CCR5 as does LL as does HIV. If LL impeded cytokine signaling as you say it does, that is, to reduce inflammation, how then is healing achieved without communication? If it is just as much as an impediment to immunocommunication as RANTES, then how is it that the immune system is so efficient when LL binds to CCR5 if there, as you say, exists no cellular communication?

Surely we can say that it is effective because it is PREVENTING CCL5 RANTES from binding and even dislodges it from the N terminus when in sufficient quantity. But we can not definitively say that it blocks/hinders/obstructs other cellular chemokine pathways.

Wouldn't it make more sense to understand that CCL5 RANTES, confounds and blocks normal immunocommunicatory signals when it binds to CCR5 because of its confomational changes it induces to CCR5 when it binds to it.

Surely, it is exactly this effect that we are witnessing which RANTES achieves when it binds to CCR5, Mass delusion and trance like states, almost at a "Stalemate" in chess when no party can make a move, but it is this way because nobody involved knows what's going on when CCL5 binds there. Because intra-cellular interleukin communication ceases with RANTES bound to CCR5.

But, when LL displaces RANTES, and takes over that binding site, all immunoregulatory communication is immediately re-established and things start working as they should, only RANTES can not bind to CCR5 anymore. Chemokines are not blocked, CCR5 maintains its shape, when LL is bound to CCR5, the signals of all the interleukins are transmitted efficiently, thereby effecting a healing response which reduces inflammation which is the design of the immune system, to restore health.