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Posted On: 11/15/2023 5:16:39 AM
Post# of 148870
That is interesting ohm.
What was it exactly that Dr. Maddon & CytoDyn actually claimed for years? That LL is a blockade of CCR5?
It totally makes sense that LL binds to the N teminus and by doing so, not only does it achieve a direct blockade of CCR5, but it also achieves an indirect blockade of the other chemokine ligands such as CCL2, CCL3, 4, 5 (RANTES), etc.. thereby preventing those ligands from binding to that N terminus on CCR5.
I appreciate your point, that leronlimab achieves this mult-faceted effectiveness because of this multi-modal mechanism of action by blocking the ligands that bind at the N terminus of CCR5 while not preventing their binding at other receptors such as CCR2, 3, etc...
That capacity to inhibit these ligands only at CCR5, but having no inhibition at the other receptors does not inhibit the adaptive immune response, but does inhibit the inflammatory cascade. By disallowing those other ligands access to CCR5 at the N terminus, the mechanism of action that leads to inflammation is inhibited, but the necessary mechanisms that leads to the appropriate adaptive immune response remains unimpeded.
Therefore, with the administration of leronlimab, patients no longer need to suffer through the terribly morbid and frequently mortal effects of the inflammation that is associated with so many disease processes. It is usually those inflammatory symptoms rather than the disease itself which does the killing or the suffering. It is the bodies own reaction to that disease which becomes the patients cause of death or becomes the patients cause of suffering. Much of that occurs before the body has had sufficient opportunity to develop the appropriate adaptive immune response, which would then be utilized to overcome the original invading pathogen.
With leronlimab, the patient can develop that appropriate adaptive response without suffering the ill effects of the typical associated inflammatory side effects. All of that happens because, the channels that are necessary to develop that inflammatory response come through "other" chemokines, other ligands that bind at the N terminus of CCR5. It becomes the varied combination of the "other" ligands which produce the varied inflammatory conditions of rash, edema, swelling, blistering, itching, thickening, induration, etc. Different diseases recruit and require different combination and quantities of the various "other" ligands.
I'm not sure I understand your last paragraph. Why are the "other" chemokines elevated? Are you saying that in a disease process, CCR5 is elevated and "ALL" the associated ligands, CCL2-5, and others are also elevated in turn? I don't see why this elevation of both the receptors and all the ligands brings it to a normal state.
What was it exactly that Dr. Maddon & CytoDyn actually claimed for years? That LL is a blockade of CCR5?
It totally makes sense that LL binds to the N teminus and by doing so, not only does it achieve a direct blockade of CCR5, but it also achieves an indirect blockade of the other chemokine ligands such as CCL2, CCL3, 4, 5 (RANTES), etc.. thereby preventing those ligands from binding to that N terminus on CCR5.
I appreciate your point, that leronlimab achieves this mult-faceted effectiveness because of this multi-modal mechanism of action by blocking the ligands that bind at the N terminus of CCR5 while not preventing their binding at other receptors such as CCR2, 3, etc...
That capacity to inhibit these ligands only at CCR5, but having no inhibition at the other receptors does not inhibit the adaptive immune response, but does inhibit the inflammatory cascade. By disallowing those other ligands access to CCR5 at the N terminus, the mechanism of action that leads to inflammation is inhibited, but the necessary mechanisms that leads to the appropriate adaptive immune response remains unimpeded.
Therefore, with the administration of leronlimab, patients no longer need to suffer through the terribly morbid and frequently mortal effects of the inflammation that is associated with so many disease processes. It is usually those inflammatory symptoms rather than the disease itself which does the killing or the suffering. It is the bodies own reaction to that disease which becomes the patients cause of death or becomes the patients cause of suffering. Much of that occurs before the body has had sufficient opportunity to develop the appropriate adaptive immune response, which would then be utilized to overcome the original invading pathogen.
With leronlimab, the patient can develop that appropriate adaptive response without suffering the ill effects of the typical associated inflammatory side effects. All of that happens because, the channels that are necessary to develop that inflammatory response come through "other" chemokines, other ligands that bind at the N terminus of CCR5. It becomes the varied combination of the "other" ligands which produce the varied inflammatory conditions of rash, edema, swelling, blistering, itching, thickening, induration, etc. Different diseases recruit and require different combination and quantities of the various "other" ligands.
I'm not sure I understand your last paragraph. Why are the "other" chemokines elevated? Are you saying that in a disease process, CCR5 is elevated and "ALL" the associated ligands, CCL2-5, and others are also elevated in turn? I don't see why this elevation of both the receptors and all the ligands brings it to a normal state.
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