Jonathan Edwards
Senior Member (Voting Rights)
It would target the NK cells just the same. The absence of many NK cells from blood doesn't necessarily mean there aren't any. They may be busy in tissues.
Preprint A Proposed Mechanism for ME/CFS Invoking Macrophage Fc-gamma-RI and Interferon Gamma, 2025, Edwards, Cambridge and Cliff
- Thread starter Nightsong
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It would target the NK cells just the same. The absence of many NK cells from blood doesn't necessarily mean there aren't any. They may be busy in tissues.
hotblack
Senior Member (Voting Rights)
Ah, so they’d still be the key strut but less visible. Interesting.
I suppose I was thinking maybe there are various routes of, say, interferon stimulation. And maybe the sum of all those is the problem. So depending upon which dial you have most ready access to, or which is most significant for a patient, you could turn that one down and let the rest of the system sort itself out. So maybe for some it was NK cells, but maybe for others some other inhibitor or strut would be better to knock out.
OrganicChilli
Senior Member (Voting Rights)
How so? Even Fluge and Mella aren't retreating non-responders even though some ended up with more NK cells after unsuccessful treatment.
V.R.T.
Senior Member (Voting Rights)
Perhaps this is a cost/showing efficacy thing and they will do this at some point if they have reason to think NK cells effect on drug action is the link/cause of the separation
Jonathan Edwards
Senior Member (Voting Rights)
The question was framed with the premise that the drug was working through NK cell gamm interferon. For all we know the reason for non-responding might have nothing to do with cell numbers - that might have been a fluke.
Timko
New Member
@Jonathan Edwards I have tried IVIG and a Jak-Stat Inhibitor. No effect. Could your theory still hold even if these treatments turn out to have no effect in a broader population? If so, what could explain such a non-response?
Jonathan Edwards
Senior Member (Voting Rights)
I would not expect IVIG to have nay effect relevant to this theory. If a Jak-Stat inhibitor blocked the effects of gamma interferon, even in hidden environments, then a lack of effect would be against the theory. On the other hand, this theory focuses on how an immune response might trigger a long term neurological response and one possibility is that effects of gamma interferon initially can outlast the presence of cytokine. We have seen at least one study suggesting that.