Figure 3.
Figure 3. IL-3-induced NKp44 expression persists during IPC culture, whereas CpG and virus block NKp44 induction. (A) Peripheral blood IPCs were cultured in the presence of IL-3. The mean fluorescence intensity (MFI) of anti-NKp44 staining was measured at 10, 21, 32, 48, and 72 hours of culture. Cells stained with control antibody fell within the horizontal bars. (B) Freshly isolated peripheral blood IPCs were cultured in IL-3-containing medium in the presence of CpG, influenza virus (WSN), or poly(I:C) (polyinosinic-polycytidylic acid). NKp44 expression was evaluated after 16 hours of culture. CpG and WSN blocked NKp44 induction, whereas the TLR3 agonist poly(I:C) did not influence NKp44 expression, consistent with the lack of TLR3 in IPCs. Cells stained with control antibodies fell outside the horizontal bars.

IL-3-induced NKp44 expression persists during IPC culture, whereas CpG and virus block NKp44 induction. (A) Peripheral blood IPCs were cultured in the presence of IL-3. The mean fluorescence intensity (MFI) of anti-NKp44 staining was measured at 10, 21, 32, 48, and 72 hours of culture. Cells stained with control antibody fell within the horizontal bars. (B) Freshly isolated peripheral blood IPCs were cultured in IL-3-containing medium in the presence of CpG, influenza virus (WSN), or poly(I:C) (polyinosinic-polycytidylic acid). NKp44 expression was evaluated after 16 hours of culture. CpG and WSN blocked NKp44 induction, whereas the TLR3 agonist poly(I:C) did not influence NKp44 expression, consistent with the lack of TLR3 in IPCs. Cells stained with control antibodies fell outside the horizontal bars.

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