IL-10 is a potent immunosuppressor produced by several immune cells [38] , and its expression can be triggered by TLR [31, 32] . IL-10 is critical in suppressing excessive inflammation and immunopathologic conditions caused by the host immune system responding to infections [39, 40] . DHF patients showed high serum levels of IL-10, which may be involved in the pathogenesis of severe dengue disease [41, 42] . In a WNV animal infection model, IL-10 downregulated T cell-mediated immunity and had a negative role in antiviral immunity [43] . Thus, our findings that DENV-2 failed to induce IL-10 expression in BMDCs (Figure 1 ) are unexpected but are consistent with previous reports that IL-10 is not produced from mature human CD1a+ DCs infected with DENV-2 [44, 45] and that microarray data from DENV-1-infected rhesus macaques showed no transcription of IL-10 or other cytokine genes [15] . In addition, we found that DENV-2 could inhibit TLR-triggered IL-10 expression. Therefore, the high IL-10 expression found in patients with dengue-related diseases might not be simply stimulated by the DENV itself. Instead, it may be resulted from uncontrolled DENV replication, which then triggers increased levels of immune activation and increased IL-10 production. DENV infection through the ADE route often induces IL-10 expression, which worsens the host anti-viral system and results in increased DENV production [35, 37, 45] . Thus, DENV infection via ADE or non-ADE routes might have different effects in the immune system.