A question remains whether the effects of IL-1 on phagocytic leukocytes is direct, or indirect via induction of other pro-inflammatory mediators such as IL-12 and IFNγ, both of which have been reported to protect against polymicrobial sepsis.32 IL-1 can directly prime neutrophils and monocytes for enhanced anti-microbial activity.33, 34, 35 However in our studies, IL-1α, IL-1β and TNFα levels were unchanged following anti-IL-1 blockade (Figure 3), suggesting an indirect effect. The gene discussed is IFNG; the disease is Sepsis.