A New Role for IL-33 in Platelet Biology
IPBS is delighted to announce the publication of groundbreaking research led by Dr. Emma Lefrançais in the journal Blood Advances, uncovering a key role for the IL-33/ST2 axis in platelet biology. The study, entitled “The alarmin Interleukin-33 modulates platelet proteome, function and biogenesis”,
reveals how the inflammatory cytokine IL-33 profoundly shapes platelet production and function.
Platelets are best known for their role in blood clotting, but they are also central players in immune regulation and inflammation. Although platelets themselves do not express IL-33, this work demonstrates that IL-33 strongly influences how platelets are made and how they behave.
Using advanced proteomics, functional assays, and lung intravital microscopy, the team shows that IL-33/ST2 signaling:
– Remodels the platelet proteome, enriching proteins involved in inflammation and immune responses,
– Impairs platelet adhesion and thrombus formation when absent, particularly under high shear stress,
– Accelerates platelet production in the lung, by promoting megakaryocyte fragmentation within the pulmonary vasculature
Importantly, the study highlights that IL-33 acts on specific subsets of megakaryocyte and hematopoietic progenitors expressing the IL-33 receptor ST2. These populations expand during stress and aging, suggesting that IL-33-driven pathways are especially relevant in inflammatory and age-related conditions.
“Our results identify IL-33 as a pivotal regulator of platelet function and production, linking inflammatory signaling to dynamic control of thrombopoiesis”, explains the research team.
This work provides new insight into how immune signals shape platelet biology and opens perspectives for targeting the IL-33/ST2 axis in thrombo-inflammatory diseases, infection, and aging.
Reference
Lucie Gelon, Stéphane Roga, Anne Gonzalez-de-Peredo, Edith Vidal, Jean-Philippe Girard, Sonia Severin, Emma Lefrançais.
The alarmin Interleukin-33 modulates platelet proteome, function and biogenesis. Blood Advances DOI 10.1182/bloodadvances.2025018363