, 2004; Rehaume et al., 2010). Very little is known regarding the pathways regulating IL-17 when encountering pathogenic microorganisms, because only artificial

conditions, such as inducing TH17 proliferation with anti-CD3/anti-CD28, have been used. A recent work identified mannose receptors as the most important pathway for IL-17 induction and TLR2/dectin-1 as having a secondary amplification effect on mannose receptor-induced IL-17 production in response to C. albicans (Van de Veerdonk et al., 2009). A study by our group (Moresco et al., 2002) demonstrated that suckling mice pretreated with concanavalin-A (Con-A) survived an intraperitoneal inoculum of 5 × 107 C.  albicans, whereas all control this website mice died within 24–48 h of infection. This effect of Con-A was attributed to IFN-γ production by direct bind to CD3 and TCR on T helper cells and subsequent increase in phagocytic and candidacidal activities of macrophages. On the other hand, IL-12 is a cytokine with links to both see more innate and adaptative immunity systems, and it constitutes an essential component of the adaptative response that leads to the generation of Th1-type cytokine responses such as IFN-γ and TNF-α (Hamza et al., 2010) and protection against disseminated candidiasis (Ashman et al., 2010).

Previously, our group reported that treatment with Con-A for 3 days protected 100% of mice against a lethal inoculum of C. albicans by increasing activity of mannose receptors on peritoneal macrophages, which produced significantly more TNF-α and were more able to kill C. albicans in vitro or over the course of infection with Candida compared to

the control group (Conchon-Costa et al., 2007; Geraldino also et al., 2010). This study tested the hypothesis that greater activity of mannose receptors and dectin-1 on peritoneal macrophages from mice pretreated with Con-A could facilitate the activation of TH1 and TH17 subsets over the course of infection by C. albicans. Candida albicans strain CR15 was isolated from the oral mucosa of a patient with HIV infection at the university hospital and maintained on Sabouraud dextrose agar; the isolate was used after two serial animal passages. C. albicans blastoconidia were obtained by growth in Sabouraud dextrose broth for 24 h at 28 °C, were washed with phosphate-buffered saline (PBS) and resuspended at 107 blastoconidia in 1 mL of RPMI 1640 (Sigma-Aldrich, St. Louis, MO). Subgroups of five male Swiss mice, each weighing 28–32 g and aged 4–6 week old, received sterilized food and water ad libitum. The mice were pretreated with 250 μg of Con-A (Sigma-Aldrich)/250 μL PBS intraperitoneally (i.p.) or 250 μL PBS alone and 3 days later were infected with 1 mL of C. albicans CR15 107 (i.p.). One group of five noninfected mice was used as control.