Seems like a big step/confirmation.  
This study provides direct evidence for the autoimmune hypothesis. Researchers found an **11-fold increase in CD4+ T-cells** specifically within the hypocretin/orexin region of the hypothalamus in NT1 brains. These T-cells express markers for **tissue-resident memory (TRM)**, such as CD49a and CXCR6.  
  
The autoimmune attack causes a selective damaging of the hypocretin/orexin-secreting cells - which do not regenerate.  It's like an injury, leaving a scar that equates to lifelong damage, as the scar prevents any recovery of the damaged region.  It's a permanent neurodegeneration strictly localized to the specific cells.

When you add in this research:  
[teams.semel.ucla.edu/sleep-research](http://teams.semel.ucla.edu/sleep-research)  
It shifts from a single-point to multi-focal failure of the wake-system which may speak into the broader spectrum of Central Disorders of Hypersomnolence - so Type 2 and IH, too.  
Speaking into the brain's main source of norepinephrine, also being significantly damaged.

Combining the two it's as though the 'master controller' (orexin), in the Hypothalamus, and a critical 'engine' (norepinephrine in the Locus Coeruleus) of wakefulness, in the brainstem, are lost.

Perhaps Type 2 Narcolepsy and Idiopathic Hypersomnia may represent restricted or localized manifestations of the same autoimmune 'ordeal' that triggers Type 1. In this framework, the damage is concentrated within the **Locus Coeruleus** (norepinephrine system) but stops short of the **Hypothalamus**, thereby sparing the hypocretin/orexin neurons from the permanent autoimmune 'scarring' and destruction seen in Type 1.

"Increased Numbers of CD4+ T-Cells in the Hypocretin/Orexin Region of Narcolepsy Type 1"