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Posted On: 11/08/2022 1:45:13 PM
Post# of 148878
Ohm20, as I know you know, Leronlimab targets no morbidity directly. (CCR5 blockade stops exploitation of CCR5 by HIV directly, of course.)
In all of the evidence we have with LL as an immune system modulator, LL tends to push the immune system into homeostasis. Therefore, wouldn't all of the "heat maps" of cytokines, if Leronlimab is able to do its job, look roughly identical? (CCR5 Delta 32 types ignored).
If the cytokine profiles of individuals given LL for a sufficient period of time are not nearly identical, that would be due to the indications themselves being treated for or a person's specific chemistry. ("Confounding factors"
Just like with blood panels, peoples' cytokine panels should be roughly similar if their health conditions are similar, especially if their immune systems are judged to be in a state of homeostasis.
Isn't that correct?
In all of the evidence we have with LL as an immune system modulator, LL tends to push the immune system into homeostasis. Therefore, wouldn't all of the "heat maps" of cytokines, if Leronlimab is able to do its job, look roughly identical? (CCR5 Delta 32 types ignored).
If the cytokine profiles of individuals given LL for a sufficient period of time are not nearly identical, that would be due to the indications themselves being treated for or a person's specific chemistry. ("Confounding factors"
Just like with blood panels, peoples' cytokine panels should be roughly similar if their health conditions are similar, especially if their immune systems are judged to be in a state of homeostasis.
Isn't that correct?
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