38 μg mL−1, Super 1) cultures induced increased (P<0.01) candidacidal activity (23%) in macrophages compared with the candidacidal activity of macrophages treated with

control (PBMC without 3M-003) supernatants (Fig. 4). IFN-γ treatment of macrophages induced significantly (P<0.01) increased killing of C. albicans (37%) (Fig. 4). Similar results were obtained in another experiment where Super 1 and Super 3 (3 μM=1.14 μg mL−1), and IFN-γ at 1000 and 250 U mL−1, all increased (P<0.01) macrophage candidacidal activity compared with killing by control macrophages. When supernatants from PBMC+3M-003 LDK378 molecular weight (3 μM) cultures were incubated with monocytes, the candidacidal activity of monocytes was significantly (P<0.05) increased, to 20%, compared with monocyte killing of C. albicans by monocytes treated with control (PBMC without 3M-003) supernatants (Fig. 5). IFN-γ (250 U mL−1) treatment of monocytes also induced increased (P<0.05) click here monocyte candidacidal activity (23%) (Fig. 5). In another experiment, supernatants from PBMC+3M-003 (3 μM, Super 3), but not Super 1 (1 μM), again increased (P<0.05) monocyte killing of C. albicans. IFN-γ (1000 U mL−1) treatment of monocytes also increased (P<0.01) the candidacidal activity of monocytes. Neutrophils were treated with supernatants from PBMC+3M-003 (1 and 3 μM, Super 1 and Super 3) cultures. Super 1 and Super 3 treatments significantly (P<0.01) increased neutrophil killing of C. albicans to

73% and 66% respectively, compared

with neutrophils treated with control supernatants (42%) (Fig. 6). Moreover, IFN-γ (250, 500, 1000 U mL−1) treatment of neutrophils significantly enhanced (P<0.01) the candidacidal activity of neutrophils to 68%, 73%, 88%, respectively, compared with control neutrophils (Fig. 6). In a second experiment, we found that supernatants from PBMC+3M-003 (3 μM) cultures or IFN-γ (250 U mL−1) treatment of neutrophils significantly (P<0.01) increased the candidacidal activity of neutrophils compared with killing of C. albicans by neutrophils treated with control (PBMC with no 3M-003) supernatants. The signaling pathway of imiquimod and related imidazoquinolines in a variety of immune and other cell types Alanine-glyoxylate transaminase through TLR-7 and TLR-8 is being defined. It involves MyD88, IRAK, TRAF6, nuclear factor-κB (NF-κB), and MAPK (Bottrel et al., 1999; Hurwitz et al., 2003; Akira & Takeda, 2004; Uematsu et al., 2005). By activation, in cells of the innate immune response (monocytes, macrophages, and dendritic cells) (Garland, 2003), of various downstream pathways, and not by direct action on T cells, these agents result in the induction of cytokines and chemokines, for example IFN-α, IFN-γ, G-CSF, GM-CSF, IL-1, MIP-1, MCP-1, TNF-α, IL-6, IL-8, IL-10, and IL-12 (Bottrel et al., 1999; Wagner et al., 1999; Dahl, 2002; Harandi et al., 2003; Gupta et al., 2004; Caron et al., 2005; Uematsu et al., 2005). This polarizes toward a T helper type 1 response.