Thisresponse differed from the IFN-γ response, and the concentration of IL-1β inplasma progressively declined, suggesting that these differences may beattributed to the response of its anti-inflammatory cytokine activities such asIL-4, IL-5, IL-10 via inhibition of the expression of IL-1β, and TNF-α [91] or as the classical pro-inflammatorycytokine cascade observed during acute inflammation, such as sepsis [92, 93]. The gene discussed is IL10; the disease is Sepsis.