Platelets, traditionally recognized for their involvement in hemostasis and wound healing, also play a central role in immune regulation and inflammation. Their function and production adapt in response to inflammatory cues such as cytokines and danger-associated molecular patterns. Interleukin-33 (IL-33), an alarmin released during tissue damage, particularly in lung inflammation, has been implicated in influencing platelet biology, though its exact effects remain poorly understood. To clarify IL-33’s role, we examined its impact on platelet proteome. We first compared the proteome of platelets purified by FACS from IL-33-deficient (IL-33KO) mice versus WT mice (n=5 biological replicates in each group, 10 raw MS files). We also compared the proteome of platelets from WT mice which were either non stimulated (n= 8 biological replicates) or treated intranasally with recombinant IL-33 (n= 9 biological replicates).