I personally think most of these HPA axis findings are superficial and haven't been properly in the depth required to lead to any sort of conclusions.
The low levels of cortisol, has long been speculated to co-exist with increased GC Receptor expression or activity (which would allow overall homeostasis to be maintained). Which is of course the opposite of GC resistance.
What do we actually know? Well studies of GC receptor expression activity, affinity etc have led to contradictory results. We should also consider the role of (low) vasopressin which has also been implicated in some of these HPA axis studies. We also know in general that there are interactions between vasopressin receptors and beta adrenal receptors. Specifically, if you had low vasopressin, then you'd expect higher vasopressin receptor expression to compensate, that would in turn inhibit beta adrenal receptor activity. There seems to be no discussion of this in the CFS literature. Interestingly, β-2 adrenergic receptor gene expression has been found to be low in several studies, but has a greater than increase in expression post-exercise, compared to sedentary controls.
The cytokine studies do tend to show a trend overall - towards an anti-inflammatory profile, with IL-10 in particular.
There is evidence for downregulated cellular stress responses/signalling cascades, despite evidence of increased oxidative stress. Expression of some of these kinase pathways directly affects the expression of genes that play a role in NK cell lytic activity.
Conclusion - there are lots of possiblities out there, some in-depth work needs to be done to uncover the overall picture.