This session will highlight four emerging topics in hemostasis and thrombosis research, each providing new and significant insights into their respective fields. The first presentation will discuss the hemostatic role of extravascular FIX in hemophilia B prophylaxis. The second presentation will focus on the conformational regulation of integrin αIIbβ3 during platelet activation and the implications for anti-platelet therapies. The third presentation will introduce a novel immune regulatory function of platelets. The fourth presentation will report findings on how F12 haploinsufficiency provides protection against venous thromboembolism.

Dr. Dargaud will discuss the role of extravascular FIX in hemophilia B. His recent findings demonstrate that, in individuals with severe hemophilia B receiving regular prophylaxis with four different FIX formulations, the progressive accumulation of FIX in the extravascular space significantly enhances coagulation capacity in specific target tissues. This process offers substantial protection against bleeding events.

Dr. Zhu will present on the central role of platelet integrin αIIbβ3 (GPIIbIIIa) in thrombosis and thrombocytopenia. His presentation will provide an overview of current knowledge regarding the conformational regulation of integrin αIIbβ3 during platelet activation and its inhibition by anti-platelet therapies. Additionally, he will delve into the structural basis of αIIbβ3 as an alloantigen in immune thrombocytopenia.

Dr. Hou will describe a novel immune regulation function of platelets. Her findings reveal that treatment with thrombopoietin receptor agonists induces platelet-derived TGF-β1, which reprograms myeloid-derived suppressor cells via the TGF-β/Smad pathway. This study aligns with growing evidence that TPO-RA treatment triggers plausible treatment-free remission in steady responders, indicating a common mechanism of immune regulation in ITP-specific therapies mediated by platelet-derived TGF-β.

Dr. Haj will report on the first large-scale analysis of the differential thrombotic risk associated with germline loss of function in the gene encoding FXII. Her research involving 415,921 individuals reveals that F12 haploinsufficiency is protective against venous thromboembolism. These findings suggest that therapeutic blockade of FXII in humans is likely to be both safe and effective.

If you are attending the meeting in San Diego, following this session, please join ASH leadership and your colleagues at the ASH Networking Reception for the Hemostasis and Thrombosis Community, taking place across the hallway, outside on the East Terrace at the San Diego Convention Center, from 6:00 p.m. - 7:30 p.m.