Negative control sections were stained with isotype immunoglobulin (Ig)G that resulted in no positive staining (data not shown) (samples were observed from all the patients described in the text). Fig. S3. Staphylococcal enterotoxin B (SEB) increases the levels of acid-related orphan receptor (ROR)γt in forkhead box P3 (FoxP3)+

regulatory T cells (Treg). Peripheral blood mononuclear cells Nutlin-3 order (PBMC) were isolated from 10 healthy subjects and cultured in the presence of SEB (10 μg/ml) for 4 days. Cells were collected at the end and analysed by flow cytometry. (a,c) Dot plots indicate CD4+ FoxP3+ Treg before (a) and after (c) culture. (b,d) Histograms indicate RORγt+ Treg (open histograms). The solid histograms MG132 indicate isotype immunoglobulin (Ig)G staining. “
“In a previous study, our group verified that 100% of mice survived to a lethal dose of Candida albicans following pretreatment with concanavalin-A (Con-A) for 3 days. This work proposed

to investigate whether treatment could mediate an adaptative immune response involving TH17 cells. A significant increase in IL-17 levels at 6 h postinfection was observed and was maintained up to 18 h in the Con-A group, whereas in control mice, a reduction in this cytokine was verified. In addition, TH17 cells develop in the presence of TGF-β, IL-1 β, and IL-6 that were increased significantly 2 h postinfection in Con-A-treated mice. Macrophages were involved in the process, engulfing greater numbers of yeast cells, and were activated through TNF-α and interferon-γ produced at significant levels at 2 h postinfection. A significant increase in IL-12 levels was also observed at 2 h postinfection. Thus, activated macrophages were probably more capable of killing and processing Candida antigens, signalizing an adaptative immune response. Macrophages from controls did not prevent yeast-to-hyphae transition and were partially destroyed, as shown

in scanning microscopy. These results suggest that treatment with Con-A many facilitated the triggering of TH17 and TH1 responses via IL-17 and IFN-γ production, leading to the resolution of C. albicans infection. Candida albicans is a commensal organism found in the gastrointestinal and reproductive mucosa; however, in immunocompromised settings, C. albicans leads to oral and oropharyngeal, vulvovaginal, mucocutaneous or disseminated candidiasis (Villar & Dongari-Bagtzoglou, 2008). C. albicans may cause peritonitis when it reaches the peritoneal cavity through iatrogenic inoculation involving contaminated plastic devices and fluids during continuous ambulatory peritoneal dialysis (Michel et al., 1994; Goldie et al., 1996; Fourtounas et al., 2006). The immune responses to these different forms of disease are quite distinct, revealing the complexity of the anatomical basis for host defenses against C. albicans infection.