First we had!
A high IL-17F concentration in the serum of people with RRMS is associated with nonresponsiveness to therapy with IFN-beta.
Then the sort of retraction that the Nature Med paper conclusions was kind of mushroom food
We were unable to validate the finding that serum IL-17F is a predictor
of PR in a large independent cohort of subjects with RRMS. Differences
in patient populations and methodology might explain the failure to
validate the results from the Stanford (Steinman) study.
Now we have
Interleukin-17 (IL-17), which is secreted by
Th17 cells, is a proinflammatory cytokine that is implicated in the
pathogenesis of multiple sclerosis (MS) and plays a role in nonresponse of MS patients to interferon-β (IFN-β) therapy.
Conclusions, RRMS
patients with high serum IL-17A levels do not respond well to IFN-β
therapy and have shorter MS duration compared to patients with low
IL-17A levels.
Interleukin 17 is a cytokine that acts as a potent mediator in delayed-type reactions by increasing chemokine production in various tissues to recruit monocytes and neutrophils to the site of inflammation, similar to Interferon gamma. IL-17 is produced by T-helper (Th17) cells and is induced by IL–23.Interleukin 17 (IL-17A) comes in different isoforms and there is IL-17B, IL-17C, IL-17D, IL-17E (also called IL-25), and IL-17F. The original idea which was later questioned was based on IL-17F not IL-17A. So is this study also not robust. This is often the problem with some original papers published in high impact journals that they spawn a lot of other studies but when the original idea is questionable it takes ages to sort out the wheat from the chaff.