Figure 2
Figure 2. Monocytes mediate IL-4–enhanced IFN-λ1 production. PBMCs were depleted of T cells, B cells, NK cells, or monocytes by magnetic bead separation. (A) Successful depletion of the indicated populations was verified using flow cytometry (percentage of remaining cells indicated; top panels). The percentage of pDCs present in each depleted population was also measured by flow cytometry (percentages indicated; bottom panels). Depleted populations were then stimulated with HSV in the presence or absence of IL-4 to determine the contribution of each cell type to enhanced IFN-λ1 production. (B) SNs were harvested after 24 hours and assayed for presence of IFN-λ1 by ELISAs (n = 4). The graph shows percentage change in HSV-induced IFN-λ1 production upon addition of IL-4. Means ± SE for the 4 donors are shown. *P < .05, determined using the Student t test.

Monocytes mediate IL-4–enhanced IFN-λ1 production. PBMCs were depleted of T cells, B cells, NK cells, or monocytes by magnetic bead separation. (A) Successful depletion of the indicated populations was verified using flow cytometry (percentage of remaining cells indicated; top panels). The percentage of pDCs present in each depleted population was also measured by flow cytometry (percentages indicated; bottom panels). Depleted populations were then stimulated with HSV in the presence or absence of IL-4 to determine the contribution of each cell type to enhanced IFN-λ1 production. (B) SNs were harvested after 24 hours and assayed for presence of IFN-λ1 by ELISAs (n = 4). The graph shows percentage change in HSV-induced IFN-λ1 production upon addition of IL-4. Means ± SE for the 4 donors are shown. *P < .05, determined using the Student t test.

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