30 Patient age and incubation time to positivity were the only independent predictors of mortality in a multivariate analysis controlling for several other known risk factors (e.g. APACHE II score, neutropenia, catheter removal). Mortality increased by 2% per hour of

incubation time elapsed. Median time to initiation of antifungal therapy after notification of culture positivity was 7 h, which indicates another delaying factor with room for improvement. The cohort analysis performed by Morrell et al. [37] previously identified delays of the start of therapy after retrieval of blood culture sample as a risk factor for hospital mortality. Delaying the initiation of therapy for more than 12 h after retrieval of the blood sample that later yields positive results was associated with almost this website threefold increase in hospital mortality (from 11% to 30%) and was identified as an independent risk factor for mortality in multiple logistic regression analysis, as Selleck STA-9090 were APACHE II score and prior antibiotic therapy. Another cohort analysis by Garey et al. [38] used different time categories and found that delays in the initiation of antifungal therapy beyond 24 h

after blood sampling significantly increased the mortality from 15% to 24% (therapy started on day 2) and 37% (day 3). The influence of timely initiation of antifungal treatment was confirmed in a neutropenic animal model. Increasing the delay in drug administration gradually reduced the therapeutic efficacy to a point at which the drug effect was completely abolished.39 Taken together, these data clearly underscore the need for early and – in septic shock – immediate initiation of therapy. The European sepsis guidelines issued in 2008 advocate the immediate Interleukin-3 receptor use of antifungals in septic shock patients at high risk of candidaemia, albeit somewhat indirectly: they argue that calculated antimicrobial therapy should be started within 1 h after recognition of septic shock or severe sepsis without shock and that clinicians should consider

whether Candida is a likely pathogen when choosing the initial regimen.40 In the light of a 33-h median time to blood culture positivity (see above), we either need innovative diagnostic tools for much earlier identification of Candida in the bloodstream or we have to enhance our ability to identify patients being at high risk of having candidaemia when developing signs and symptoms of systemic infection. The difficulties of identifying patient groups at high risk are illustrated by a recent prospective randomised trial. Schuster et al. [41] compared empirical fluconazole with placebo in ICU patients deemed at risk for IC. Inclusion criteria were: ICU stay of ≥96 h, APACHE II score of ≥16, 4 days of fever, broad-spectrum antibiotics for ≥4 days and presence of a central venous catheter.

Using a visual fixation procedure, the present study tested whether French-learning 14-month-olds have the knowledge of syntactic categories

of determiners and pronouns, respectively, and whether they can use these function words for categorizing novel words to nouns and verbs. The prosodic characteristics of novel words stimuli for noun versus verb uses were balanced. The only distinguishing Alisertib cue was the preceding determiners versus subject pronouns, the former being the most common for nouns and the latter the most common for verbs, i.e., Det + Noun, Pron + Verb. We expected that noun categorization may be easier than verb categorization because the co-occurrence of determiners with nouns is more consistent than that of subject pronouns with verbs in French. The results showed that infants grouped the individual determiners as one common class, and that

they appeared to use the determiners to categorize novel words into nouns. However, we found no evidence of verb categorization. Unlike determiners, pronouns were not perceived as a common syntactic class. “
“Young children begin helping others with simple instrumental problems from soon after their first birthdays. In previous observations of this phenomenon, both naturalistic and experimental, children’s parents were in the room and could potentially have influenced their behavior. In the two current studies, we gave 24-month-old children the opportunity to help an unfamiliar adult obtain an out-of-reach object when the parent (or a friendly female adult) (i) was present but passive, learn more (ii) was present and highlighted the problem for the child, (iii) was Methocarbamol present and actively encouraged the child to help, (iv) was present and ordered the child to help, or (v) was absent from the room. The children helped at relatively high levels and equally

under all these treatment conditions. There was also no differential effect of treatment condition on children’s helping in a subsequent test phase in which no parent was present, and children had to disengage from a fun activity to help. Young children’s helping behavior is not potentiated or facilitated by parental behavior in the immediate situation, suggesting that it is spontaneous and intrinsically motivated. “
“Research suggests that nonlinguistic sequence learning abilities are an important contributor to language development (Conway, Bauernschmidt, Huang, & Pisoni, 2010). The current study investigated visual sequence learning (VSL) as a possible predictor of vocabulary development in infants. Fifty-eight 8.5-month-old infants were presented with a three-location spatiotemporal sequence of multicolored geometric shapes. Early language skills were assessed using the MacArthur-Bates CDI.

Some Treg cells also infiltrate germinal centers to negatively regulate TFH cells and this Ulixertinib process would lead to higher affinity B-cell responses [[20, 21]]. Finally, mast cells also directly activate B cells to induce IgA production via CD40L, IL-6, and IL-10 [[121]]. This activation

may contribute to TI IgA responses in the intestinal lamina propria. Basophils, an innate cell type closely related to mast cells, also deliver helper signals to B cells via both direct and indirect mechanisms (Fig. 4). Firstly, under certain circumstances, basophils can migrate to draining lymph nodes where they release IL-4 to induce the formation of TH2 cells, an IL-4-producing T-cell subset critically involved in the induction of protective IgG1 and IgE responses against various mTOR inhibitor allergens and pathogens, including helminths [[122-125]]. Secondly, after secondary immunization, basophils recognize antigen through prebound antigen-specific IgE generated during a primary immune response [[126]]. Antigen recognition via IgE causes upregulation of CD40L and release of IL-4 and IL-6, which provide antibody-inducing

signals to B cells not only directly, but also indirectly via enhancement of IL-4, IL-6, IL-10, and IL-13 production by TH2 cells [[112, 126]]. Presumably, the antigen-IgE interaction does not trigger pathological release of preformed highly inflammatory compounds, such as histamine, from basophils owing to the low affinity

of IgE for antigen. It must be also noted that IgE can also bind DCs, which raises the possibility that DCs could account for at least part of the Th2-inducing activity ascribed to basophils [[127]]. Basophils may deliver similar B-cell helper signals by interacting with IgD (Fig. 4), an enigmatic antibody isotype released by IgD class-switched plasmablasts originating in the human upper respiratory mucosa [[52, 128]]. In spite of being heavily hypermutated, these IgD antibodies are largely polyreactive and may afford mucosal protection by binding not only to commensals and pathogens but also to their virulence factors [[52, 83, 129, 130]]. In addition to crossing the epithelial barrier to reach the surface of upper respiratory mucosal surfaces, IgD binds to circulating basophils, monocytes, and neutrophils, as well PRKACG as mucosal mast cells, via an unknown receptor [[52]]. Crosslinking of prebound IgD induces basophil release of BAFF, IL-4, and IL-13, which in turn stimulate B cells to undergo IgM production, as well as CSR to IgG and IgA, in a TI manner [[52]]. CD40L and APRIL further help the activation of B cells by IgD-activated basophils [[52]]. Thus, basophils may utilize both prebound IgE and IgD as immune amplifiers of both systemic and mucosal B-cell responses. TFH cells, TFR cells, NKTFH cells, and Treg cells play a pivotal role in TD antibody responses against microbial proteins.

42 Reports of transient HBsAg seropositivity after vaccination exist. Most likely this is vaccine-induced, spurious, and persists for up to 20 days.43 No action is required assuming the HBsAg serology

is negative once again after 3 weeks. In the 1970s, Krugman observed that HBsAg was immunogenic, and that anti-HBs antibodies were protective against hepatitis B.44 Napabucasin clinical trial A first-generation vaccine was subsequently developed, consisting of HBsAg extracted by plasmapheresis from HBV carriers, and then inactivated.45 This vaccine, manufactured by Merck, was approved by the Food and Drug Administration in 1981, and became widely available from July 1982. A similar vaccine was licensed at about the same time, produced by Institut this website Pasteur in France. Modern ‘second-generation’ HBV vaccines are recombinant non-infectious subunit vaccines containing HBsAg.46 These are produced by the yeast Saccharomyces cerevisiae using recombinant DNA technology. There are two such HBV vaccine formulations available, Engerix B and Recombivax HB. A third-generation vaccine has been produced from a mammalian cell line, although it is not yet in widespread use. It contains the pre-S1 and pre-S2 antigens that

are present on the viral envelope. These antigens are more immunogenic than the HBsAg present in second-generation vaccines.47 Whichever vaccine is used, providing manufacturer’s recommendations are adhered to, immunogenicity and efficacy are considered equivalent.48 In line with Krugman’s earlier observations, efficacy studies have shown that at least 90% of subjects developing anti-HBs levels of 10 IU/L are protected from hepatitis B infection.49 Safety data are comprehensive. A large prospective trial has shown the vaccine to be safe and well-tolerated.50 Szmuness et al.51 demonstrated the efficacy of the first-generation, plasma-derived HBV vaccine (PDV) in 1980 in a randomized, double-blind placebo-controlled Sitaxentan trial (RCT) in a high-risk population with normal renal function. The same group then investigated use of the Merck vaccine in 79 US HD patients and demonstrated that 89% produced detectable anti-HBs.10

The Pasteur vaccine was examined in an RCT of 138 dialysis patients. Despite a low seroconversion rate of 60%, the vaccine was protective when compared with placebo (Table 2).52 Another observational study of the Merck vaccine found seroconversion rates of 50% in male HD patients and 66% in females. By contrast, 100% of seven pre-dialysis patients had protective antibody.53 Szmuness’ group reported the largest RCT of HD patients in 1984 (n = 1311).54 A three-dose schedule produced a 50% response rate. Two other early studies found seroconversion rates in HD patients of 60–75%.11,55 The second, a Dutch RCT, replicated the findings of the prior French study,52 showing that the vaccine was protective against HBV infection compared with placebo.

CD39-positive Tregs increased during ECP treatment compared to HTxC. ECP-treated patients showed higher levels for T helper type 1 (Th1), Th2 and Th17 cytokines. Cytokine levels were higher in HTx patients with rejection before ECP treatment compared to patients MK0683 with prophylactic ECP treatment. We recommend a monitoring strategy that

includes the quantification and analysis of Tregs, pDCs and the immune balance status before and up to 12 months after starting ECP. “
“Galectin-9 (Gal-9) plays pivotal roles in the modulation of innate and adaptive immunity to suppress T-cell-mediated autoimmune models. However, it remains unclear if Gal-9 plays a suppressive role for T-cell function in non-autoimmune disease models. We assessed the effects of Gal-9 on experimental hypersensitivity pneumonitis induced by Trichosporon asahii. When Gal-9 was given subcutaneously to C57BL/6 mice at the time of challenge with T. asahii, it significantly suppressed T. asahii-induced lung inflammation, as the levels of IL-1, IL-6, IFN-γ, and IL-17 were significantly reduced in the BALF of Gal-9-treated mice. Moreover, co-culture of anti-CD3-stimulated CD4 T cells with BALF cells harvested from Gal-9-treated mice on day 1 resulted

in diminished CD4 T-cell proliferation and decreased levels of IFN-γ and IL-17. CD11b+Ly-6ChighF4/80+ Ku-0059436 ic50 BALF Mϕ expanded by Gal-9 were responsible for the suppression. We further found in vitro that Gal-9, only in the presence of T. asahii, expands CD11b+Ly-6ChighF4/80+ cells from BM cells, and the cells suppress T-cell proliferation and IFN-γ and IL-17 production. The present results indicate that Gal-9 expands immunosuppressive CD11b+Ly-6Chigh Mϕ to ameliorate Th1/Th17 cell-mediated hypersensitivity pneumonitis. Galectin-9 (Gal-9), a β-galactoside binding lectin, is a ligand for T-cell immunoglobulin- and mucin domain-containing molecule 3 Casein kinase 1 (Tim-3), which plays crucial roles in innate and adaptive immunity via Gal-9/Tim-3 interactions 1, 2. Tim-3 is expressed

on terminally differentiated Th1 cells, Th17 cells and innate immune cells, such as DC 2–4. Gal-9 induces apoptosis of activated Th1 and Th17 cells, in part, through the Ca2+-calpain-caspase1 pathway 5, resulting in the amelioration of immunopathology in murine autoimmune disease models such as collagen-induced arthritis (CIA), autoimmune diabetes, and EAE 2, 6, 7. Little is known, however, as to whether mechanisms other than apoptosis of Th1/Th17 cells are involved in Gal-9-mediated suppression of inflammation. We have shown, for example, that Gal-9 also enhances Treg generation from naïve CD4+ T cells in a murine CIA model 7. Although we have previously shown that Gal-9 induces DC maturation 8 and weakly promotes TNF-α production from DC 2, it has been widely accepted that certain types of Mϕ/DC, including myeloid-derived suppressor cells (MDSC) and regulatory DC (DCreg), also exhibit immunosuppressive function in a variety of immune responses 9–11.

0001) or other hospital patients (P < 0.0001). In addition, their arterioles (mean difference

−18.0 μm, 95%CI −12.88 to −23.08, P < 0.01) and venules (mean difference −25.3 μm, 95%CI −17.09 to −33.52, P < 0.01) were narrower. Microvascular retinopathy was still more common in patients with OSA, and arteriolar and venular narrowing persisted after adjusting for age, BMI, mean arterial pressure, smoking and dyslipidemia. Conclusions: Patients LY2157299 concentration with OSA have more small vessel disease than those with COPD and other hospital patients, with worse microvascular/hypertensive retinopathy and narrower vessels. 180 WHAT IS THE HEALTH LITERACY OF RENAL PATIENTS ? RESULTS OF A CROSS SECTIONAL STUDY K LAMBERT1, M LONERGAN1, P RUSSELL1, K MURALI1, J MULLAN2, K MANSFIELD2 1Illawarra Shoalhaven Local Health District, Wollongong, NSW; 2Graduate School of Medicine, University of

Wollongong, Wollongong, NSW, Australia Aim: To investigate the prevalence of low health literacy in a cross sectional sample of peritoneal dialysis (PD), haemodialysis (HD) and kidney transplant patients. Background: Health Literacy is the ability to seek, understand and utilise health information. Low health literacy is associated with poorer health outcomes. There is limited research regarding the health literacy of renal patients or on the use of the Health Literacy Management Scale (HeLMS). This relatively new tool, unlike other health literacy tools, allows researchers to investigate more thoroughly the domains of seeking, understanding and utilising health information. Methods: Ethics approval was Selleckchem LY2606368 granted from the local ethics committee. Invitations to participate were sent to 92 HD, 46 PD and 145 transplant patients. Exclusion criteria included patients with known dementia or cognitive impairment based on formal assessment. Health Literacy was assessed using the HeLMS tool. Results: Recruitment is ongoing. To date, 65 patients have been assessed (n = 30 HD, n = 24 PD and n = 11 transplant patients). Preliminary analysis indicates

no significant differences between groups for total scores in each of the eight health literacy domains measured. Sub Chlormezanone group analysis indicates that PD patients score significantly lower on the domains of ‘reading written information’ (P = 0.03) and ‘reading health information’ (P = 0.04). Moreover, 31% of HD patients and 59% of PD patients reported ‘difficulty finding the motivation to manage their health’. Finally, more than 40% of each of group reported difficulty ‘understanding health information’. Conclusions: Many renal patients struggle to understand health information and to manage their health. How this impacts on self management requires further investigation. Further longitudinal studies in these groups and in those approaching dialysis is also required.

After 4 hr the numbers of cells migrated to the bottom wells or not were determined by flow cytometric analysis of the content of the bottom wells and the inserts, respectively, on a FACSCalibur (BD Biosciences). The migration rate was calculated by division of the number of cells in the bottom well by the total number of cells present in the insert and in the bottom well. As a control, the number of cells added to the inserts was determined by flow cytometric analysis on

a FACSCalibur (BD Biosciences). 5 × 106 BMDCs d8 were loaded with 2 µM fluo-3 AM with an excitation maximum at 506 nm and an emission maximum at 526 nm (Molecular Probes, Leiden, Ceritinib purchase the Netherlands) in supplemented RPMI 1640 medium for 20 min. After washing for two times with fresh medium in supplemented RPMI 1640 medium were seeded at a density

of 1 × 106 BMDCs in uncoated six-well plates and stimulated or not with 500 ng/mL LPS up BMS-777607 supplier to 4 hr. At the indicated time points 1.25 × 105 cells were harvested and 2000 cells each were analyzed for the mean Ca2+-dependent fluo-3 AM fluorescence intensity (excitation wave length 488 nm, detection wave length 530 nm) on an LSRFortessa™ cytometer using FACSDiva™ software version 6.1.3 (both from BD Biosciences). 1 × 106 BMDCs d8 in supplemented RPMI 1640 medium were seeded in uncoated 24-well plates (Greiner Bio-One) and stimulated or not with 500 ng/mL LPS (Calbiochem) for 4 hr. Thereafter, cells were harvested, centrifuged (400g, 5 min), and the pellet was resuspended in 50 µL PBS. After addition of 0.5 µg biotin-conjugated anti-mouse CCR7 clone 4B12 (eBioscience,

Frankfurt, Germany) and 0.2 µg APC-labeled anti-mouse CD11c (HL3) (BD Pharmingen 550261, Heidelberg, Germany) antibodies cells were incubated for 30 min on ice. After washing with PBS cells were resuspended in 50 µL PBS and incubated with 0.5 µg Streptavidin-PE antibodies (BD Pharmingen 554061) for 30 min on ice to detect binding of the biotin-conjugated CCR7 antibodies. After washing with PBS cells were analyzed by an LSRFortessa™ cytometer using FACSDiva™ software version 6.1.3. The expression CCR7 on BMDCs was determined by gating on double-positive (CD11c+/CCR7+) cells. The unpaired two-tailed O-methylated flavonoid Student’s t-test was used to evaluate differences in means between two groups. P-values were considered statistically significant if *P < 0.05, **P <0.01, or ***P < 0.001. LPS signaling can induce maturation and migration of DCs [7]. Additionally, it has been described that cell swelling is essential for N-formyl-methionyl-leucyl-phenylalanine (fMLP)-induced migration of human polymorphonuclear leukocytes [12]. Additionally, swelling of DCs has been observed after treatment with LPS for 4 hr [13]. Hence, in order to analyze the role of TLR4 signaling in LPS-induced cell volume changes, we analyzed cell volume changes of immature WT and TLR4−/− BMDCs at different time points after addition of LPS.

The endoscopic insertion of plastic stents represents an effective system of biliary decompression contributing to the regression of symptomatology and determining a significant improvement of quality of life in patients suffering from obstructive jaundice associated with malignant hepatobiliary tumors or benign strictures (Ballinger et al., 1994). However, the major limitations of this palliative approach are mainly represented by stent occlusion, often followed by life-threatening cholangitis necessitating repeated interventions and stent exchange.

Stent occlusion is caused by the deposition of biliary sludge, which is composed of cholesterol crystals, calcium bilirubinate and palmitate, amounts of cholesterol as well as bacteria and/or fungi, microbial byproducts, proteins, dietary fibers and glycoproteins Metformin (Dowidar et al., 1991; McAllister et al., 1993; Weickert et al., 2001; Moss et al., 2006; Donelli et al., 2007). Deposition of calcium salts due to the biochemical activities of bacterial enzymes in the biofilm growing on the surface of the stents and reflux of intestinal contents into stents have been proposed Selleckchem BMN673 as the two main mechanisms of stent occlusion (Speer et al., 1988; Moesch et

al., 1991; Sung et al., 1993). However, some authors suggested that microbial adhesion and biofilm formation on the surface of the stent lumen could play an important role in the initiation of the clogging process and in the subsequent stent blockage (Leung et al., 1988, 2000; Basoli et al., 1999; Di Rosa et al., Venetoclax in vivo 1999; van Berkel et al., 2000, 2005; Guaglianone et al., 2008). Microorganisms gain access into the biliary system either by descending via the portal venous circulation or by ascending through the

sphincter of Oddi in duodenal–biliary reflux (Sung et al., 1992). Bacteria adhere to the stent surface and their sessile growth and exopolysaccharide production lead to the establishment of a thick biofilm conferring microorganisms with an efficient protection from both antibacterial agents and phagocytic cells. The β-glucuronidase and lecithinase (or phospholipase C) enzymatic activities of colonizing microorganisms lead to the precipitation of calcium bilirubinate and palmitate, thus contributing to the sludge accumulation within the biliary system and then to the stent occlusion (Leung et al., 1988). The aims of this study were to analyze the biliary sludge of 28 clogged stents to check the presence of ex vivo biofilm formation, to identify all the microbial species colonizing the stents’ lumen and to verify the in vitro ability of isolated anaerobic bacteria to form a biofilm. Twenty-eight clogged biliary stents were removed from patients (mean age=66 years) who had undergone endoscopic stent insertion for the treatment of a variety of diseases involving biliary obstruction. The implantation time ranged from 20 to 484 days (mean=164).

The objective of this study was to assess whether peptidoglycan (PGN) derived from Gram-positive bacteria induces trophoblast stem (TS) cell death or alters TS cell cytokine

production. Method of study  Toll-like receptor (TLR) transcript expression was assessed by RT-PCR. Protein expression was determined by confocal microscopy or flow cytometry. 7-Aminoactinomycin D (7-AAD) staining was used to assess TS cell death. Morphological features of cell death were evaluated by transmission electron microscopy. The presence of cleaved caspase-3 and high mobility group box 1 (HMGB1) protein was examined by Western blot. Cytokine levels PLX4032 purchase in cell supernatants were determined using a mouse cytokine 23-plex panel. Results  Toll-like receptor 2 and TLR4 protein was expressed from the 1-cell stage through the blastocyst stage of murine embryo development. Murine TS cells expressed TLR2 and TLR6 but not TLR1 or TLR4 RNA. Only TLR2 protein was detected at the plasma membrane of TS cells.

PGN induced TS cell death by a caspase-3-independent mechanism. The cell death pathway induced by PGN was morphologically consistent with necrosis. Finally, PGN induced HMGB1 release Daporinad clinical trial and increased MIP-1β secretion while inhibiting the constitutive release of RANTES. Conclusion  Peptidoglycan-induced TS cell necrosis and the subsequent Parvulin release of HMGB1 and MIP-1β may regulate an infection-induced inflammatory response at the maternal–fetal interface and thus may play a role in the pathogenesis of infection-associated pregnancy complications. “
“A good understanding of the immunological correlates of protective immunity is an important requirement for the development of effective vaccines against malaria. However,

this concern has received little attention even in the face of two decades of intensive vaccine research. Here, we review the immune response to blood-stage malaria, with a particular focus on the type of vaccine most likely to induce the kind of response required to give strong protection against infection. Malaria still causes serious illness and many deaths in some of the poorest countries in the world. Over 200–300 million new cases are reported each year with 1·2 million deaths, mainly of young children [1]. There is still no vaccine that confers strong protective immunity to infection. Gaps in our understanding both of putative vaccine antigens and of the nature of antimalarial immunity have held back the development of a protective vaccine. While some immunity is acquired to infection after several years of repeated exposure to malarial infection, it is never complete. Such partial immunity or naturally acquired immunity that does develop, in an age and exposure related manner, involves both antibody and cell-mediated immune responses.

We next analysed the effect of bromelain in combination with the cytokine cocktail. Because cytokine cocktail stimulation resulted in the most mature phenotype and stimulation with bromelain lead to a higher IL-12p70 secretion, we were interested to find out whether an additive or synergistic effect could be detected. We also tested bromelain combined with two modified versions of the cytokine cocktail containing less or no PGE2 as it has been stated that PGE2 is responsible for the lack of IL-12p70 production [17, 18]. The phenotype of the cells revealed that all DC populations

stimulated with a combination of bromelain and the cytokine cocktail (original cocktail, ¼ of PGE2 and without PGE2) had a mature phenotype (Fig. 2), selleck kinase inhibitor but the population with the least mature phenotype among these was the group that was stimulated with bromelain and the cytokine cocktail without any PGE2 (Fig. 2). The DC populations stimulated with bromelain in combinations with the cytokine cocktail and the cytokine cocktail with ¼ of PGE2 showed an even more mature phenotype compared with cytokine DC, with the highest CD86, CD80, CD83 and CCR7 surface expression (Fig. 2). Interestingly, a synergistic effect was detected on CD83 and CCR7 surface expression when bromelain was added to the original or modified cytokine

cocktail with ¼ PGE2. We also analysed the migratory potential of the generated DC populations but could not detect any clear differences between the populations ICG-001 (data not shown). Removal of PGE2 from the cytokine cocktail resulted in reduced surface levels for most of the markers analysed compared with the original cytokine cocktail (Fig. 2). When ¼ of PGE2 was included in the cocktail, the surface expression was restored (Fig. 2). We also determined the MFI of these many markers (Fig. 2B). All populations expressed comparable amounts of CD40. The density of surface CD38 was highest upon treatment with bromelain alone or in combination with the modified cytokine cocktail without PGE2. Treatment

of the cells with the modified cytokine cocktail without PGE2 resulted in lowest surface expression of HLA-DR, similar to that of immature cells. HLA-DR was highest expressed on DC treated with a combination of bromelain and the cytokine cocktail (Fig. 2B). DC stimulated with a combination of bromelain and the cytokine cocktail did only produce higher amounts of IL-12p70 when PGE2 was completely removed from the cocktail (Fig. 3). However, this DC population had a less mature phenotype (Fig. 2). As expected, immature DC and DC stimulated with the cytokine cocktail alone did not produce considerable amounts of IL-12p70. To analyse the functionality of the generated DC populations, we performed allogeneic MLR to assess the T cell stimulatory capacity. As shown in Fig. 4, immature DC had, as expected, the lowest capacity to stimulate allogeneic T cells.