Ohm has a handle on this more than most, and his e
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Posted On: 05/14/2025 2:00:42 PM
Re: sherlock57 #152859
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Ohm has a handle on this more than most, and his emphasis on “homeostasis” has been very helpful to me in grasping a hint of the contingency and complexity of all this. His comment in a post a few days ago about a CC5 receptor “retreating” into a cell just blew my mind.
When a ligand (CCL5 et al.) binds to its receptor it activates intracellular proteins that cause the effects the ligand is programmed to do. It then either degrades or if needed can return to the surface of the cell to bind another ligand. Since leronlimab doesn't activate intracellular proteins it will stay on the surface and block all ligands or the HIV virus.
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I wonder if the promotion of homeostasis by leronlimab is one reason we have what appear to be cures in mTNBC?
Normally the immune system would destroy aberrant cells like tumor cells. When presented with an immune challenge the tumor cells preferentially switch the environment to one where M1 macrophages (anti-inflammatory, anti-cell destruction) predominate and cell protectors like PD-L1 proliferate. Leronlimab changes things over to an M2 macrophage type (killer T cells) and reduces cell protecters. Which is how things should be so homeostasis.
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Well Cassandra, the emphasis in your post about CCL5 signaling made me think we should probably be paying more attention to that side of the equation. I recall a comment by Bruce Patterson, back in 2020 TED TALK I believe, who famously said “Covid-19 was a RANTES disease…”
What if metastasis turns out to be a RANTES disease? What if atherosclerosis is a RANTES disease? Fibrosis? AD?
Saying that they are RANTES (CCL5) diseases is not quite right. The underlying causes are usually genetic, environmental or viral/bacterial. RANTES and the cascade of effects from it can play a role in greatly worsening disease states and RANTES is preeminent in the immune space with it preferentially binding CCR5. However other ligands and proteins also take part.
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