This table of results is interesting:
What it seems to show is almost definitional. There are many differences in the early stages between typical onset ME/CFS and atypical, but they tend to converge.
You can observe that by the number of bolded p values in the second comparison column: 18. That column compares classical onset and atypical onset patients who've only had the disease a short time. A lot of differences!
But in the second last column (which compares long-duration patients who had classical vs atypical onsets) we see only three cytokines of 55 with statistically significant differences. Much more similar.
So over time, the differences between atypical and classical are decreasing. Which matches what I observe on this forum. People complain about different things, but there are few or no obvious links between what our problems are and how we got the disease
One obvious difference in the table is IL17A, which I highlighted. It has some seriously low p values and seems to consistently show difference over time between classical and atypical. I'd like to know more about what it does!
The conclusion says the overall level of cytokines is lower in atypical than classical, (although without a healthy control group I'm not sure whether that implies the atypical folk have depressed immune systems or the classical ones do?)
"Although few differences were apparent in cytokine levels across the different subsets within the A-ME/CFS subgroup, the atypical group as a whole had markedly lower levels of several inflammatory cytokines as compared with C-ME/CFS patients. Although some differences were noted in CSF cytokines based on duration of illness—a factor we previously found to profoundly affect plasma cytokine levels in ME/CFS in prior work12— adjustment for illness in our final logistic regression models did not eliminate findings of inhibited inflammatory cytokines in A-ME/CFS."