In conclusion, our results demonstrate that CD8<sup>+</sup> T cells and IFN-γ are associated with autoimmune myelofibrosis, a finding that may allow targeting of CD8<sup>+</sup> T cells and IFN-γ as a therapeutic targets.
The striking deregulation of IFI genes may reflect a hyperstimulated but insufficient immune system being most enhanced in patients with advanced myelofibrosis, in whom the IFI27 gene displayed an exceedingly high expression.