Consistently, the protective mAb significantly attenuated sepsis-induced systemic accumulation of IL-6, sTNF-RI, and several chemokines (e.g., MIP-1γ, MIP-2/GRO-β, and KC/GRO-α; Fig. 8C), suggesting that these beneficial antibodies confer protection against lethal sepsis possibly by attenuating sepsis-induced dysregulated inflammation. This evidence concerns the gene CXCL2 and Sepsis.