natasa778
Certainly the Th17 immune response (which is activated by IL-17) does serve a purpose, and I think that's why Dr Lipkin sounds a note of caution regarding the idea of inhibiting Th17 and IL-17 in ME/CFS patients.
So you wouldn't want to issue any general advice to ME/CFS patients to reduce their Th17 + IL-17 responses just yet.
Though I am always quite happy to experiment on myself: there is a mad scientist on the ethics committee of my personal n = 1 study trials — me — and that mad scientist usually gives the ethical go ahead for many unorthodox or unproven treatment ideas to be tested on myself! Though I am also the first to instantly halt any such trails at any signs that hint of untoward side effects.
In terms of the purpose of Th17: the Th17 immune response comes into play when fighting Staphylococcus bacteria (especially in the skin), Salmonella enterica in the gut, and Candida albicans. Th17 may also play a role in fighting Tuberculosis, and Borrelia bacteria, but not enough is known about this role to make any definitive statements in these cases. The discovery of the Th17 immune response is fairly new, so not that much is known about it, in comparison to the Th1 and Th2 immune responses.
From the ME/CFS perspective, the fact that Th17 significantly increases the levels of coxsackievirus B infection in a murine myocarditis model should be cause for concern. From Dr John Chia's work, we know that ME/CFS is characterized by a persistence, smoldering enterovirus infection that, in ME/CFS patients, does not seem to go away, and is not cleared by the immune system. So the million dollar question is:
what is preventing or impeding the clearance of enteroviruses like coxsackievirus B in ME/CFS patients?
The conventional answer to this question is that the low Th1 response (antiviral response) and the high Th2 response found in ME/CFS patients act to prevent enteroviral clearance in the body, hence the use of Th2 => Th1 immunomodulators like oxymatrine, in order to boost the Th1 antiviral response, and achieve viral clearance. But as we know from Chia's research, such immunomodulators only seem to work well for a subset of ME/CFS patients. So what is blocking the effects of these Th2 => Th1 immunomodulators in the majority of ME/CFS patients that don't seem to respond to immunomodulators like oxymatrine?
Well, what if there were other factors, such as a high Th17 response, that were also standing in the way of viral clearance? We know from the
references cited above that Th17 + IL-17 act to increase enterovirus infections in a murine myocarditis model; so Th17 is acting against enteroviral clearance. It is conceivable that if you not only addressed the Th1 deficiency in ME/CFS patients, but also addressed this Th17 that may be blocking viral clearance, then you might successfully treat ME/CFS.
So conceivably, you may have a better chance of clearing the enterovirus infections driving ME/CFS if you used both Th2 => Th1 immunomodulators like oxymatrine
and Th17 suppression immunomodulators at the same time.
Though this idea may be more appropriate in the first year or two of developing ME/CFS, where Dr Lipkin found that IL-17 is high.