Sorry, the proposed reason for non-classical monoc

Sorry, the proposed reason for non-classical monocyte persistence is given in the paper, and I should have reviewed again since I read it last week:

Quote:

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It has been shown in both humans and mice that nonclassical monocytes require fractalkine (CX3CL1) and TNF to inhibit apoptosis and promote cell survival22. Our previous data show high IFN-γ levels in PASC individuals5, which can induce TNF-α production23. Further, TNF-α and IFN-γ induce CX3CL1/Fractalkine production by vascular endothelial cells24 creating the conditions to promote survival of nonclassical monocytes.

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I guess just having all those non-classical monocytes persisting because of high TNF-alpha and fractalkine (and low CCL4/CCR5 based migration) is the reason for PASC. That's why BP recommended also using a statin to lower fractalkine. Inhibiting CCR5 might cause more intermediate monocytes to turn into harmful non-classical, inflammatory monocytes, but LL could block those existing cells traveling throughout the body and causing widespread damage.

Quote:

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Previously, CD16+ monocytes were demonstrated to migrate into the brain of AIDS patients expressing high levels of CX3CL1 (fractalkine) and SDF-126, and mediate blood-brain barrier damage and neuronal injury in HIV-associated dementia via their release of proinflammatory cytokines and neurotoxic factors. These sequelae are very common in PASC and these data could represent the underlying mechanism for the symptoms.

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So on one hand LL could create more non-classical monocytes (by keeping the intermediate monocytes in the blood), but on the other hand, LL might prevent the existing cells from going throughout the body (brain, heart, etc...) and causing damage there.

Sorry for thinking out loud, and not giving it more thought before the first post. Would love to hear others' ideas.

Also can't wait to see what Recknor is up to in the lab, and how it fits into the pathogenic and therapeutic puzzle.