Ala Altaie: We Found That Mononuclear Cells From RA Patients Can Trigger Clot Formation
Ala Altaie, Research Fellow in Mesenchymal Stem Cell Biology at the Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, shared a post on LinkedIn:
”New paper out!
Why do some patients on JAK inhibitors develop venous thromboembolism (VTE) or pulmonary embolism (PE) without deep vein thrombosis?
In our latest study led by Paula David and colleagues, we found that mononuclear cells from RA patients can trigger clot formation—especially when exposed to JAK inhibitors like tofacitinib.
This process, known as immunothrombosis, links the immune system to coagulation through increased Factor III production.
Panel A: Clots formed faster with tofacitinib
Panel B: Clot strength was higher
These findings shed light on the immune–coagulation connection behind JAK inhibitor–associated clots.
Read more.”
Title: Augmentation of immunothrombosis as a key mechanism underlying JAK inhibition associated hypercoagulability in rheumatoid arthritis
Authors: Paula David, Tom Macleod, Ala Altaie, Yu Shi, Kerem Abacar, Sami Giryes, Gabrielle de Mello Santos, Payal Ganguly, Mark Harland, Chi Wong, Andrew Scarsbrook, Paul Emery, Kulveer Mankia, Shouvik Dass, Andrea Di Matteo, Benazir Saleem, Cédric Duval, Robert Ariëns, Dennis McGonagle
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