pattismith
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I don't think Chlamydia downregulates P2X7. On the contrary!Would it then be expected that Chlamydia may downregulate P2X7, and that could explain the temporary improvement?
P2X7 activation is an answer to Chlamydia infection that protects the host and lead to lowering of the chlamydial load.
So what I understand from these papers is that Chlamydia can show up when P2X7 is underactive (when ME/CFS has a break for unknown reason).
The other hypothesis could be that Martin has a problem to clear Chlamydia because of a failure of P2X7 activation, which resolves from time to time (for example if P2X7 is activated by LPS from gut bacteria), leading to clearance of the skin problem, lowering of the chlamydia load and producing the rising of the ME/CFS.
The thing that we don't know yet is if an intracellular low grade chlamydia persistence could trigger some persistent immune activation (with elevated TNF alpa and/or activated P2X7)
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