Sepsis is typically initiated by bacterial infection and the associated immune dysregulation displays a complex, dynamic biphasic immune response characterized by hyperinflammation followed by immunosuppression. In the initial period, pathogens activate the innate immune system through receptors such as Toll-like receptors (TLRs) and NOD-like receptors (NLRs), resulting in the massive release of cytokines, including IL-1β, IL-6, and IFN-γ, thereby initiating a "cytokine storm" that leads to vascular endothelial damage, complement activation, and the induction of abnormal cellular aggregation. Sustained activation of inflammatory signals initiates inflammasome-mediated cell death, including pyroptosis-apoptosis-necroptosis (PANoptosis), leading to systemic inflammation and organ dysfunction. Later, the host develops an immunosuppressive phase characterized by increased anti-inflammatory mediators (e.g., IL-10 and TGF-β), exhaustion of B, T, and NK cells, and immune checkpoint-mediated immune paralysis. The stepwise progression of these two stages suggests that sepsis is not simply a consequence of uncontrolled inflammation but rather reflects immune system reprogramming. A better understanding of the molecular basis of inflammation and immunosuppression, particularly the crosstalk among cell death pathways, metabolic reprogramming, and immune regulation, may facilitate timely precision interventions and the restoration of host immune homeostasis in sepsis.