Longitudinal multi-omic profiling of sepsis reveals that clinical stage of illness is frequently asynchronous with underlying immune-state trajectories. Distinct STImS immune states are marked by coordinated shifts in T-cell checkpoint expression (PD-1, PD-L1, CTLA4), B-cell/plasma-cell modules including BAFF-receptor (TNFRSF13C) hubs, and circulating cytokines such as APRIL, BAFF, sCD40L, IL-6 and IFN-γ. These programs provide translational opportunities to align immunotherapy timing with immune state rather than calendar disease stage.
