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Posted On: 06/09/2022 4:30:18 AM
Post# of 148899
The long and the short of this is the fact that Metastasis requires the Primary Tumor to over express CCL5 RANTES. CCL5 RANTES creates the opposite response from our own immune cells that we would other wise expect. Instead of killing the Primary Tumor, our white blood cells are "educated" / "hypnotized" to understand that the Primary Tumor is "Self" and not to be destroyed. In addition to that, our Immune System is controlled to induce the development of blood vessels to the Primary Tumor to help it grow. All Circulating tumor cells, (Metastasis) that are put forth from the Primary Tumor are "Protected" and not gobbled up. The are given free pass to pass through the wall of the circulatory system and enter the blood stream from where they may travel through the body and Metastasize to another area.
The only way the Primary Tumor gets away with this is through RANTES, CCL5 overexpression binding to upregulated CCR5 receptors. Where ever there is CCL5 upregulation, there will also be an induced overexpression of CCR5 on the surfaces of the the Immune Cells, the Macrophages, the Natural KIller Cells, CytoToxic T Cells, CD4, CD8 and T Regulator Cells.
T regs are the suppressors of the immune system. If they feel that the antigen is self, they turn off the immune response. Their main job is to protect self. The rest of the immune system can not tell whether the antigen is self or non self. So it relies on T regs. If T regs say the antigen is self, the remainder of the immune system leaves it alone.
T regs have CCR5 all over them. Mass CCL5 binding to all those CCR5 receptors and the T regs are happy as a pig in mud. With the mass binding of CCL5 to the numerous CCR5 receptors on the surface of T Regs, and the T Regs believe that the Primary Tumor's Circulating Tumor Cells are self. The T Regs begin telling the rest of the immune system not to kill these Circulating Tumor Cells.
The Primary Tumor accomplishes it's goal of Metastasis by gaining control of the T Regulatory - T suppressor cells. After it gains control of that master suppressor of the immune system, it has control over the entire immune system. It does this by one primary means, the over expression of RANTES or CCL5.
Leronlimab binds to CCR5 with far higher affinity than RANTES. When LL is administered, RANTES no longer can bind to CCR5 and the "hypnotizing" effects that RANTES produces cease. T Regs begin to understand that the Circulating Tumor Cells are really from the Primary Tumor and NOT self. That causes the T Regs not to miscommunicate to the Natural Killer Cells that the CTC in front of them is really self and NOT to kill it. No, instead, they say, this is "not self" and the NKC destroys it.
When LL Is given, RANTES is worthless, and VEGF is no longer expressed and the circulation to the Primary Tumor dries up and the Primary Tumor loses it's blood supply and eventually dies. The Circulating Tumor Cells killed and prevented from entering the blood stream through the walls of the circulatory system.
Why does RANTES confound when it binds to CCR5? Because RANTES is shaped in such a way that when it binds to CCR5, it presses upon the binding sites of other chemokines and interleukins and prevents other communication pathways that are necessary to continue with in the cells of the immune system. When RANTES binds, other receptors and other paths of immunocellular intracellular communication cease and therefore, the interleukin, intracellular communication ends and the immune cells don't know what's up from what's down.
When LL binds, it is a humanized monoclonal antibody and when it binds to CCR5, it does not interfere with the deeper receptors hidden beneath or around CCR5 and there by disrupt other paths of intracellular communication. When LL binds to CCL5, normal immunoregulatory control is restored with normal intracellular communication. Proper recognition of self from non self is restored.
Metastasis depends on faulty immunoregulatory control mediated by RANTES. LL is the answer to prevent Metastasis. LL also aids by cutting off the blood supply to the Primary Tumor.
However, the Primary Tumor does not express all that many CCR5 receptors on the cells of the Primary Tumor. Therefore, another drug such as a PD-1 receptor blocker may do better, although, when a CCR5 receptor exists on a Primary Tumor cell, LL will bind to it and perform PD-1, PD-L1 and PD-L2 blockade itself, there just isn't sufficient expression of CCR5 on the surfaces of Primary Tumors, so another drug is necessary to eradicate Primary Tumor.
Therefore the combination of LL with PD receptor blockade will result in a magnificent combination NON-CHEMO therapy which may be employed to eradicate the vast majority of cancer as all utilize RANTES for metastasis.
The only way the Primary Tumor gets away with this is through RANTES, CCL5 overexpression binding to upregulated CCR5 receptors. Where ever there is CCL5 upregulation, there will also be an induced overexpression of CCR5 on the surfaces of the the Immune Cells, the Macrophages, the Natural KIller Cells, CytoToxic T Cells, CD4, CD8 and T Regulator Cells.
T regs are the suppressors of the immune system. If they feel that the antigen is self, they turn off the immune response. Their main job is to protect self. The rest of the immune system can not tell whether the antigen is self or non self. So it relies on T regs. If T regs say the antigen is self, the remainder of the immune system leaves it alone.
T regs have CCR5 all over them. Mass CCL5 binding to all those CCR5 receptors and the T regs are happy as a pig in mud. With the mass binding of CCL5 to the numerous CCR5 receptors on the surface of T Regs, and the T Regs believe that the Primary Tumor's Circulating Tumor Cells are self. The T Regs begin telling the rest of the immune system not to kill these Circulating Tumor Cells.
The Primary Tumor accomplishes it's goal of Metastasis by gaining control of the T Regulatory - T suppressor cells. After it gains control of that master suppressor of the immune system, it has control over the entire immune system. It does this by one primary means, the over expression of RANTES or CCL5.
Leronlimab binds to CCR5 with far higher affinity than RANTES. When LL is administered, RANTES no longer can bind to CCR5 and the "hypnotizing" effects that RANTES produces cease. T Regs begin to understand that the Circulating Tumor Cells are really from the Primary Tumor and NOT self. That causes the T Regs not to miscommunicate to the Natural Killer Cells that the CTC in front of them is really self and NOT to kill it. No, instead, they say, this is "not self" and the NKC destroys it.
When LL Is given, RANTES is worthless, and VEGF is no longer expressed and the circulation to the Primary Tumor dries up and the Primary Tumor loses it's blood supply and eventually dies. The Circulating Tumor Cells killed and prevented from entering the blood stream through the walls of the circulatory system.
Why does RANTES confound when it binds to CCR5? Because RANTES is shaped in such a way that when it binds to CCR5, it presses upon the binding sites of other chemokines and interleukins and prevents other communication pathways that are necessary to continue with in the cells of the immune system. When RANTES binds, other receptors and other paths of immunocellular intracellular communication cease and therefore, the interleukin, intracellular communication ends and the immune cells don't know what's up from what's down.
When LL binds, it is a humanized monoclonal antibody and when it binds to CCR5, it does not interfere with the deeper receptors hidden beneath or around CCR5 and there by disrupt other paths of intracellular communication. When LL binds to CCL5, normal immunoregulatory control is restored with normal intracellular communication. Proper recognition of self from non self is restored.
Metastasis depends on faulty immunoregulatory control mediated by RANTES. LL is the answer to prevent Metastasis. LL also aids by cutting off the blood supply to the Primary Tumor.
However, the Primary Tumor does not express all that many CCR5 receptors on the cells of the Primary Tumor. Therefore, another drug such as a PD-1 receptor blocker may do better, although, when a CCR5 receptor exists on a Primary Tumor cell, LL will bind to it and perform PD-1, PD-L1 and PD-L2 blockade itself, there just isn't sufficient expression of CCR5 on the surfaces of Primary Tumors, so another drug is necessary to eradicate Primary Tumor.
Therefore the combination of LL with PD receptor blockade will result in a magnificent combination NON-CHEMO therapy which may be employed to eradicate the vast majority of cancer as all utilize RANTES for metastasis.
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