Hypothalamus antibodies, HPA-axis dysfunction and a role for NO, CO, and H(2)S in ME?

From Invest in ME’s homepage:
Invest in ME are working with researchers, as part of the examinations facility proposal and to support the rituximab trial, on a more comprehensive and detailed analysis of antibodies binding the hypothalamus.

This is interesting and wonderful news, and I hope this study will help to make the ME puzzle pieces fit together. I have written a little about it in my previous blogpost - in Danish, sorry- remember "google translate" is a fine invention: Har ME patienter auto antistoffer mod hypothalamus???

There are an abundance of articles about ME and Hypothalamic-Pituitary-Adrenal Axis (HPA-Axis) function. Could antibodies against “something” in the hypothalamus explain the HPA-Axis dysfunctions?

Hypothalamic–pituitary–adrenal axis dysfunction in chronic fatigue syndrome

Does hypothalamic–pituitary–adrenal axis hypofunction in chronic fatigue reflect a "crash" in the stress system?

The role of hypocortisolism in chronic fatigue syndrome

A Review of Hypothalamic-Pituitary-Adrenal Axis Function in Chronic Fatigue Syndrome

And will antibodies binding the hypothalamus explain some other hypothesis and observations?

Lately, I have been very interested in the role of nitric oxide (NO), carbon monoxide CO), and hydrogen sulfide H(2)S in the etiology of ME and POTS. Blogposts about it:

Basic knowledge NO - H(2)S - CO interaction - where to begin

ME/CFS, POTS - carotid body and gasotransmitters

ME, POTS, H(2)S, NO - hvad er sammenhængen?

Hydrogen sulfide, ME/CFS, POTS and TRPA1

And my suspicion to dysregulation of NO, CO, and H(2)S in ME and POTS has grown stronger after reading this article:

Roles of nitric oxide, carbon monoxide, and hydrogen sulfide in the regulation of the hypothalamic–pituitary–adrenal axis:

“The importance of NO, CO, and H(2)S in the regulation of the stress axis is beyond dispute, but their specific roles include complex interactions with one another and effects that vary with the characteristics of the stress and type of cell/organisms involved.“

The big question is how this information adds up with Decreased oxygen extraction during cardiopulmonary exercise test in patients with chronic fatigue syndrome?

Any suggestions?