IL1B and Sepsis: Early in sepsis, levels of inhibitory cytokines such as TGF-β and IL-10 increase markedly alongside proinflammatory mediators (e.g., IL-1, IL-6, TNF-α), resulting in an “inflammatory–anti-inflammatory storm.” This early release of TGF-β and IL-10 serves as a compensatory mechanism to counteract excessive inflammation [31].