Aortic & peripheral vascular disease
Inhibition of JAK-STAT Signaling Suppresses Pathogenic Immune Responses in Medium and Large Vessel Vasculitis
Authors' conclusion
Cytokine signaling dependent on JAK3 and JAK1 is critically important in chronic inflammation of medium and large arteries. The JAK inhibitor tofacitinib effectively suppresses tissue-resident memory T cells and inhibits core vasculitogenic effector pathways.
Study context
- Population
- Human arteries engrafted into immunodeficient mice reconstituted with T cells and monocytes from patients with giant cell arteritis
- Comparison
- Tofacitinib vs vehicle
- Outcome
- Vessel-wall immune responses and vasculitic lesions (T-cell proliferation and effector cytokines, angiogenesis, intimal hyperplasia, tissue-resident memory T cells) in human arteries engrafted into mice
Methodological detailshumanized mouse model (human arteries engrafted into immunodeficient mice)
- Humanized mouse model (human arteries engrafted into immunodeficient mice)
Main finding
As reported in the abstract
Lesional T-cell proliferation rates reduced with tofacitinib
<10%
Original publication
Inhibition of JAK-STAT Signaling Suppresses Pathogenic Immune Responses in Medium and Large Vessel Vasculitis. Circulation. Published 18 December 2017. doi:10.
Summarised from the published abstract; every number is checked against it