CpG-ODN was shown to be the most effective TLR agonist to prevent the development of Th2 response [15] and IL-10 production was required to shape CpG-ODN adjuvant activity, since in IL-10-deficient mice, sensitization to OVA with alum and CpG-ODN resulted in OVA-induced Th1-dominated immune responses with increased IFN-γ production and neutrophilic lung inflammation [15,16]. This evidence concerns the gene IL10 and inflammation.