To establish that the phenotype of the IL-6−/− mice was directly attributable to the actions of IL-6 and not due to other hematological changes known to occur in the IL-6−/− strain [24], we also depleted WT BALB/c mice with the anti-IL-6 monoclonal Ab 20F3 and found that Ag-specific Th2 responses to infection (as measured by IL-4 and IL-10) were elevated in treated mice MLNCs (Fig. 2D). Here, IL4 is linked to infection.