IL1B and Sepsis: For example,IL-1β, IFN-γ, or TLR signals can upregulate MHC-II and immune modulators in MKs, promotingan MK1-like phenotype [57], whereas IL-6 or TGF-βfavors platelet-generating MK2-like features [58].The inflammatory phase may further influence MK subset dynamics: MK2 predominates duringacute infection, supporting coagulation and neutrophil activation, whereas MK1 becomes moreprominent during chronic or recovery stages to mediate immune regulation—consistent with ourfindings in PICS and sepsis.