IL1B and systemic inflammatory response syndrome: Activated intrahepatic monocytes rapidly shift toward a pro-inflammatory phenotype, exhibiting elevated levels of pro-inflammatory markers such as CD80, CCR2, and the antigen-presenting molecule HLA-DR, along with an enhanced ability to release inflammatory cytokines such as TNF-α, IL-1β, and IL-6.[3] These cytokines further activate peripheral monocytes, contributing to systemic inflammatory response syndrome (SIRS) and extrahepatic organ damage.