Strikingly, while IFN-γ production was suppressed potently, an increase in IL-17+ T cells was observed [84]. These

data suggest that Th17 and Th1 cells may differ in their susceptibility to Treg-mediated suppressive signals. The pivotal influence of Tregs in determining whether a pathological autoimmune response develops following immune challenge was confirmed using Treg depletion and reconstitution strategies in various induced models of organ-specific autoimmune disease, including collagen-induced arthritis (CIA) [85] and experimental INCB024360 autoimmune encephalomyelitis (EAE) [44,86–88]. In these models depletion of Tregs was associated with more vigorous immune responses and particularly increased

levels of IFN-γ production [87], illustrating that Tregs suppress Th1 responses effectively which, at the time, were considered the driving force in these models. An elegant series of experiments dissecting the comparative roles of IL-12 and IL-23 in promoting autoimmunity prompted a dramatic change in emphasis, highlighting the pathogenic roles of IL-23 in promoting the expansion of IL-17-producing effector T cells and their critical importance in autoimmune inflammation [89,90]. Most studies using anti-CD25-mediated Treg depletion strategies were carried out before the implications of these studies click here were realized fully. However, there is evidence that Tregs suppress production of both Th1 and Th2 responses in models of arthritis [91], and that Treg depletion heightens production of IL-17 and IL-6 (both associated with Th17 responses) as well as IFN-γ during EAE [92]. Thus, it appears that Tregs have at least some capacity to hold the development of Th17 responses, as well as Th1 and Th2 responses, in check. Most models of organ specific autoimmunity are associated with definitively

Branched chain aminotransferase polarized immune responses. Unusual in this respect is autoimmune gastritis (AIG), which can be induced by Th1-, Th2- or Th17-polarized CD4+ T cells. Pathology in AIG is orchestrated by CD4+ T cells recognizing the alpha chain of the H+K+adenosine triphosphatase (ATPase) expressed in gastric parietal cells [93]. Disease can be induced in immunodeficient nude mice by transfer of antigen-specific transgenic T cells and this can be suppressed by the co-transfer of Tregs[94]. It has now been shown that while Th1, Th2 and Th17 polarized populations can all induce AIG, they differ in their pathogenicity and in their susceptibility to suppression. Th1 cells appear to be those suppressed most easily by freshly explanted polyclonal Tregs, while Th2 cells were slightly less well controlled [95].

The number of Fas+ cells was similar in the two ATL lesions but differed from healthy mucosa (Tables S1 and S2; Figure 3c). FasL+ cells presented a heterogeneous distribution in all groups studied, forming clusters close to vessels and glands. No difference was observed between ATL lesions. However, a significant difference in Caspase inhibitor the distribution/mm2 between lesion and healthy tissue was detected (Table S2; Figure 3d). In all samples, CLA+ cells were heterogeneously distributed in the lamina propria, with a higher concentration in the reticular portion and close to vessels and glands. The number of CLA+ cells in C–N was about half of that observed in ATL lesions. Differences were also observed between

ATL–O and C–O. However, there was no difference between ATL lesions (Tables S1 and S2; Figure 3e). Expression of NOS2 was observed in all groups but varied from small cell clusters (discrete) to diffuse distribution throughout all or most of the tissue (intense) (Figure 1e). Despite the wide variation LY2157299 in vitro in the intensity of NOS2 expression, large positive areas were observed in 41·7% of the cases of ATL–N but only in 14·3% of ATL–O (Figure 3f). Low expression

of NOS2, with discrete expression and distribution, was observed in clinically healthy tissues. Because of this heterogeneous distribution, a significant difference was only observed between ATL–N and C–N (Figure 3f). Correlation analysis between the detection of parasites and intensity of NOS2 expression in lesions showed an inverse correlation between the two parameters (P = 0·043). Endothelial cells expressing E-selectin (CD62E) were observed in all samples. In some fields, activated vessels were found close to nonactivated vessels. Low expression of E-selectin was observed in most control mucosa samples. No difference in the distribution of activated vessels was observed between ATL–O and C–O or between ATL–N and ATL–O. However, there was a significant difference between ATL–N and C–N (Figure 3g). In this study, we characterized the in situ inflammatory

response of oral and nasal ATL lesions to analyse the inflammatory profile in mucosal ATL. Our results showed that both oral and nasal ATL lesions selleck compound presented a marked inflammatory infiltrate mainly consisting of T cells, macrophages and, at a lower proportion, B lymphocytes and neutrophils. The predominance of T lymphocytes and macrophages has been demonstrated in ATL mucosal and cutaneous lesions (6,8–17) as well as in other infectious and noninfectious diseases, such as paracoccidioidomycosis (18), periodontitis, sinusitis, infectious rhinitis (19–22), lupus erythematosus and lichen planus (23,24). This predominance might result from the inflammatory process, which mainly stimulates cellular immune responses. In addition, a larger number of CD4+ T cells compared to CD8+ T cells was observed in ATL lesions.

Further research also confirmed that miR-155 may participate in the LPS-induced negative feedback regulation through inhibition of FADD, IKKϵ, and Ripk1 gene expression.[21] Pexidartinib in vivo This finding suggests that miR-155 plays a negative regulatory role in the LPS-mediated immune response. On the other hand, miR-155 can also promote the translation of TNF-α, which implies the underlying functional complexity of miR-155 in immune

regulation.[22] In this study, it was demonstrated that in contrast to miR-146a and miR-155, miR-451 was significantly downregulated following xenotransplantation. This indicates that miR-451 has a different regulatory effect from miR-146a and miR-155 in the process of xenograft rejection. Some studies have reported that miR-451, regulated by GATA-1,[23] plays a key role in the maturation of red blood cells through the regulation of its target gene GATA-2.[24] Rasmussen et al.[25] also found that a miR-451 deficiency would delay erythroblast maturation, resulting in erythroid hyperplasia, splenomegaly, and anemia. In addition, Zhang et al.[26] have found that overexpression of miR-451 can also provide protection against ischemia/reperfusion-induced cardiomyocyte death and augment cardiomyocyte survival. In GSK 3 inhibitor this view, we speculate that the formation of intravascular thrombosis, as the critical factor affecting heart

graft survival, is closely related to the downregulation of miR-451 at the endpoint of rejection. It has also been reported that Tollip is a predicted target gene

of miR-451 and a ubiquitin-binding protein that can interact with some components of the TLR signaling—an important inflammatory signaling regulatory factor that is closely related to CYTH4 the IL-1R and IRAK-1 activation.[27] Recently, Rebl et al.[28] found that Tollip is a negative regulator of TLR signaling. As described above, although there is a negative regulatory mechanism between miR-146a/miR-155 and TLR that plays an important role in the initiation of the immune response and pathogen recognition, we speculate that the changes of miR-451 level may facilitate the process of immune response in xenografting. In summary, at both 24 hours and at the endpoint of rejection following mouse-to-rat cardiac xenografting, 31 intragraft expressed miRNAs that may be associated with the regulation of immune responses following xenotransplantation were detected. This study has expanded our knowledge regarding the role of miRNAs in xenograft rejection, and the evidence generated deserves further investigation for the future development of clinically applicable strategies in the diagnosis, prevention, and treatment of xenograft rejection. The authors thank Yujie Qiu, Na Zhao, Hui Liang, and Yiling Hsu for technical support.

In addition, the entire contents of the resuspended biofilm were plated onto LB10 agar supplemented with 300 μg mL−1 of rifampicin (Sigma Aldrich) to quantify the number of spontaneous rifampicin-resistant mutants. The plates were incubated for 2 days at 37 °C after which time CFUs were enumerated. The mutation frequency was calculated as the number of spontaneous rifampicin-resistant mutants divided by the total viable population. The ability of each variant to utilise different see more substrates as carbon sources was determined using the commercially available

BIOLOG GN2 plates (Biolog, CA) according to the manufacturer’s instructions (minor modifications as below). Each plate contains 95 different carbon sources, each conjugated to a tetrazolium

dye. The ability to utilise a specific substrate results in dye cleavage and the formation of a purple hue in the wells. In brief, bacterial cultures were grown overnight in 10 mL of M9 medium (supplemented Everolimus with 5.5 mM glucose) at 37 °C with shaking. Following centrifugation (4580 g) and washing (twice with 10 mL PBS), bacteria were resuspended in 20 mL of GN2 inoculating fluid (Biolog). The BIOLOG GN2 plates were then inoculated with 150 μL of the resuspended bacteria and incubated at 37 °C. The OD600 nm was taken at 0, 4, 8 and 24 h (Wallac Victor2 plate reader; Perkin Elmer) to monitor the growth of cells within each well. A dye release profile corresponding to the amount and types of carbon sources metabolised was generated for the 24-h time point. The quantification of attachment Megestrol Acetate and batch biofilm formation was conducted on both polystyrene- (hydrophobic) (Sarstedt Inc) and tissue culture–treated (hydrophilic) (Costar, Corning Inc) 96-well microtitre plates using an assay similar to that described previously (O’Toole & Kolter, 1998; Pratt & Kolter, 1998; Koh et al., 2007). Briefly, for attachment, 100-μL aliquots of overnight cultures in LB10 were added into the wells, while for biofilm formation, overnight cultures were diluted 1 : 100 in LB10 broth. Subsequently, 100-μL aliquots of the diluted cultures were added into the wells,

and the plates were incubated without agitation at 37 °C for 2 h for attachment and/or 24 h with shaking for biofilm formation. After incubation, the cell density of each well was determined (OD600 nm), the cell suspensions were removed, the wells were washed twice with PBS, 100 μL of filtered 1% (w/v) crystal violet (CV) solution was added into each well, and the plates were incubated at room temperature for 20 min. The CV solution was removed, and the wells were washed three times with PBS followed by the addition of 100 μL of HPLC-grade absolute ethanol (Univar) to extract the CV for quantification at OD490 nm. For the attachment assay, the CV reading was normalised using the cell density reading (OD490 nm/OD600 nm).

001); controls had a coronary calcium score of 0 (IQR 0). Black race remained a significant negative predictor for coronary calcification after adjustment, prevalence ratio = 0.14 and 95% confidence interval (CI): 0.0–0.53. Vascular

calcification was not associated with any ambulatory blood pressure parameter. Using receiver operator characteristic curves, an abdominal aorta calcification score of ≥1 showed an area under the curve of 0.83 to predict a coronary calcium score ≥ 10. Conclusion:  Black race appears to protect from vascular calcification in South African CKD-5D patients and this warrants further study regarding https://www.selleckchem.com/products/17-AAG(Geldanamycin).html the underlying mechanism. The abdominal X-ray is a useful screening tool for coronary calcification. “
“Aim:  Continuous ambulatory peritoneal dialysis (CAPD) is a major form of therapy for chronic end stage renal disease patients, which may lead to CAPD-associated peritonitis. The spectrum of organisms associated with CAPD peritonitis varies geographically. Not much data is available regarding this from southern India. The aim of this study was to characterize the spectrum of organisms associated with CAPD peritonitis in

Buparlisib solubility dmso this region and observe the utility of automated blood culture systems to culture peritoneal dialysate. Methods:  Ninety episodes of peritonitis were cultured over a span of 3 years using an automated blood culture system. Results:  The yield of culture positivity was 50%. The most predominant organism was found to be coagulase-negative Staphylococcus spp. (21.1%) followed by Enterobacteriaceae (12.2%). Other organisms isolated were non-fermenting Gram-negative bacilli (4.4%), Pseudomonas aeruginosa (3.3%), α-haemolytic Streptococci (3.3%), Gemcitabine purchase Candida spp. (2.2%), Staphylococcus aureus (1.1%), β-haemolytic Streptococci (1.1%) and Micrococci (1.1%). A high degree of resistance to third generation cephalosporins (66.7%) was noted amongst the Gram-negative bacilli. Also, all the Gram-negative bacilli isolated from patients who had prior empirical antibiotic therapy of ceftazidime before arrival at

the centre, were resistant to third generation cephalosporins. Conclusion:  A varied spectrum of organisms isolated from peritoneal dialysate compared to the global scenario was observed. Also, a high degree of third generation cephalosporin resistance was noted amongst the Gram-negative bacilli. Thus, it is suggested that the empirical therapy should be dependent on the local epidemiology. “
“Preterm birth (birth prior to 37 completed weeks of gestation) may occur at a time when the infant kidney is very immature and nephrogenesis is often ongoing. In autopsied preterm human kidneys and in a baboon model of preterm birth it has been shown that nephrogenesis continues after preterm birth, with a significant increase in the number of glomerular generations and number of nephrons formed within the kidney after birth.

We find that LKB1 is required for several key metabolic processes in T-cell progenitors. For example, LKB1 controls expression of CD98, a key subunit of the L-system aa transporter and is also required for the pre-TCR to induce and sustain the regulated phosphorylation of the ribosomal S6 subunit, a key regulator of protein synthesis. In the absence of LKB1 TCR-β-selected thymocytes this website failed to proliferate and did not survive. LBK1 was also required for survival and proliferation of peripheral T cells. These data thus reveal a conserved and essential role for LKB1 in the proliferative responses

of both thymocytes and mature T cells. “
“The mechanisms underlying Japanese encephalitis virus (JEV) pathogenesis need to be thoroughly explored to delineate therapeutic approaches. It is believed that JEV manipulates the innate and adaptive compartments of the host’s immune system to evade Dabrafenib molecular weight immune response and cross the blood–brain barrier. The present study was thus designed to investigate the functional modulation of DCs after exposure to JEV and to assess the consequences on CD4+ T-lymphocyte functions. Human monocyte-derived DCs were either infected with 1 MOI of live virus, UV-inactivated

virus, or were mock-infected. Replication-competent JEV induced a significant increase in the expression of maturation markers 48 h postinfection, along with that of programmed cell death 1 ligand 1 (PD-L1; also called B7-H1 and CD274). JEV-infected DCs expanded the Treg cells in allogenic mixed lymphocyte reactions. The expansion of Treg cells by JEV-infected DCs was

significantly reduced upon blocking PD-L1 using an antagonist. In addition, JEV-infected DCs significantly altered the proliferation and reduced the polarization of Th cells toward the Th1-cell phenotype. The results, for the first time, Glycogen branching enzyme suggest that JEV evades the host’s immune system by modulating the crosstalk between DCs and T lymphocytes via the PD-L1 axis. “
“In this study, we elucidated the role of tumor necrosis factor (TNF)-α in the host defense to pulmonary infection with Streptococcus pneumoniae and defined the cellular source of this cytokine at an early stage of infection. Administration of anti-TNF-α monoclonal antibody (mAb) resulted in the reduced accumulation of neutrophils in bronchoalveolar lavage fluids (BALFs) and severe exacerbation of this infection. In a flow cytometric analysis, the intracellular expression of TNF-α was detected in Gr-1bright+ and Gr-1dull+ cells during the time intervals postinfection, and F4/80+ cells expressed intracellular TNF-α before Gr-1dull+ cells appeared. The Gr-1bright+ and Gr-1dull+ cells sorted from BALF cells at 24 h were identified as neutrophils and macrophage-like cells, respectively, and the Gr-1dull+ cells expressing CD11c, partially CD11b and a marginal level of F4/80 secreted TNF-α in in vitro cultures.

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 check details (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 FK506 clinical trial 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., oxyclozanide 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).

In brief, nTreg were isolated, using the MACS® protocol

(see above), from peripheral blood samples taken at 08:30 hr, which were then incubated at 37° in 5% CO2 for 30 min with 1 μg/ml of Simulect® (Novartis, Basel, Switzerland), a CD25-neutralizing antibody. nTreg were then washed twice with phosphate-buffered saline (PBS) and used for functional assays as described above. To analyze whether hormone levels at the time of T-cell isolation influenced Tres and nTreg activities, we measured cortisol, melatonin, prolactin, growth hormone and noradrenalin levels in serum or plasma using commercially available assays. For cortisol and growth hormone analysis the Immulite® system was used (Immulite; DPC-Biermann GmbH, Bad Nauheim, Germany). Prolactin was measured using an immunoradiometric assay (Prolactin IRMA; DPC-Biermann GmbH) Selleck Pembrolizumab and melatonin was measured using a radioimmunoassay (Bühlmann Laboratories

AG, Schönenbuch, Switzerland). Noradrenalin was analysed using standard high-performance liquid chromatography with subsequent electrochemical detection (Chromsystems, Munich, Germany).34 In order to investigate whether the correlational data obtained regarding the influence Palbociclib of hormones on Tres cytokine secretion can be proven in an in vitro system, we isolated Tres, using the MACS protocol (see above), from peripheral blood collected at 08:30 hr. These purified PAK5 Tres were then incubated (37°, 5% CO2) for 2 hr with physiological serum levels of cortisol (12 μg/dl; Sigma-Aldrich, Munich, Germany), melatonin (50 pg/ml; Sigma-Aldrich), or prolactin (20 ng/ml, R&D, Munich, Germany) in X-VIVO 15. After incubation, cells were washed twice, cultured as described above and the supernatants collected for analysis of cytokine concentrations. To ensure that the subjects slept well in the sleep condition, sleep quality was monitored using polysomnographic electroencephalogram (EEG) recordings.

EEG measurements were analyzed according to previously published standards.32 The mean time for sleep onset was 22·6 ± 5·6 min. Sleep time was 451 ± 6·2 min: time in stage 1 sleep was 26·3 ± 4·1 min; time in stage 2 sleep was 236 ± 23·1 min; time in slow wave sleep (SWS) was 77·8 ± 10·5 min; and time in rapid eye movement (REM) sleep was 76·8 ± 9·8 min. Latencies (with reference to sleep onset) were 19·3 ± 5·2 min for SWS and 172·1 ± 36·8 min for REM sleep. In all six subjects, SWS predominated during the first half of the night (49·3 ± 5·5 min versus 28·5 ± 9·6 min for the first half of the night and the second half of the night, respectively), while REM sleep dominated during the second half of the night (7·9 ± 2·6 min versus 70·3 ± 8·5 min for the first half of the night and the second half of the night, respectively). Hence, all subjects slept normally during the night of the experiment.

Supernatants of T-cell proliferation cultures were harvested at 48 h after initiation of culture. Concentrations of IFN-γ, TNF-α, IL-2, IL-4, and IL-5 were measured by mouse Th1/Th2 cytokine bead array assay (BD Bioscience) according to manufacturer’s recommendation. Thymus was obtained from 6-wk-old C57BL/6 mice, and cell suspensions

were stained for 15 min in PBS+0.5% BSA with specific mAbs against CD4-PE and CD8-FITC (BD Bioscience). After staining, cell suspensions were washed and resuspended for analysis. Flow cytometric analysis was performed by a FACScan (BD Bioscience). Splenic T cells from C57BL/6J mice Pictilisib concentration were starved in RPMI1640 + 0.1% FBS at 37°C and 5% CO2 for 4 h at the cell concentration of 1 × 106/mL. After the starvation, cells were resuspended in RPMI1640 + 0.1% bovine serum albumin (BSA), and seeded in the plates precoated with anti-CD3/ephrin-Bs

at 2 × 105 cells/well. The plates were centrifuged at 350 rpm for 3 min to achieve rapid contact between the cells and the bottom of the culture wells. The cells were incubated at 37°C and 5% CO2 for 2 h. Then, the cells were harvested and washed with ice-cold PBS. Cell lysis and subsequent Western blotting were performed AZD0530 chemical structure as previously described [[58]] with minor modifications. Briefly, cells were lysed in cell lysis buffer containing 50 mM Tris-HCl, pH 7.5, 150 mM NaCl, 1% Triton X-100, 1 mM sodium vanadate, 50 mM sodium fluoride, and protease inhibitor cocktail (Sigma Aldrich). For immunoprecipitation, RIPA lysing buffer (50 mM Tris-HCl, pH 7.5, 137 mM NaCl, 2 mM EDTA, 1% NP-40, 0.1% SDS, 0.5% sodium deoxycholate, 1 mM sodium vanadate, 50 mM sodium fluoride, and protease inhibitor cocktail) was used. The lysates were boiled with SDS-loading buffer. Equal amount of sample proteins (35 μg) were separated on 7.5–16% SDS-PAGE and transferred onto PVDF membranes (Immobilon, Millipore, Billerica, MA, USA). The membranes were first incubated with TBST (20 mM Tris-HCl,

second pH 7.5, 137 mM NaCl, 0.1% Tween20) containing 5% nonfat dried milk and probed with specific antibodies using primary and horseradish peroxidase-conjugated goat anti-rabbit secondary antibodies (Cell Signaling Technologies, Danvers, MA, USA). Immune complexes were detected by chemiluminescence (Immobillon Western, Millipore). For immunoprecipitation, total cell lysates were incubated with anti-PY antibody (clone 4G10, Millipore) and protein G-sepharose (GE Healthcare Bio-Sciences AB, Sweden) for 18 h at 4°C. The immunoprecipitates were washed with lysis buffer and then with PBS. The blotting membranes were incubated with biotinylated rabbit anti-goat IgG (BA-5000, Vector Laboratories, Burlingame, CA, USA) followed by the amplification with ABC system (Vectastain Elite ABC Reagent, Vector Laboratories).

For a long time, DCs have been shown to contribute to the polarization of the immune response, to elicit an efficacious host defence. However, besides this essential immunostimulatory function of DCs, consolidated findings showed that DCs may act as pivotal players in the peripheral tolerance network by active induction of immunosuppressive T cells and regulation of T-effector cell activity. To understand whether DCs play a role in the tolerance and/or subsequent immunosuppressive mechanisms that occur within the

peritoneal cavity of AE-infected mice, we addressed see more whether these cells were activated. Previous studies with other helminth models had shown that DCs did not display any new phenotype following stimulation with respective parasite antigens (ES-62, SEA, glycan LNFPIII); thus, DC-dependent Th2 immunity appeared to result from antigen GPCR Compound Library order presentation in the absence of DC maturation (12). Furthermore, it has also been previously shown that immature DCs did not mature upon exposure to unfractionated metacestode proteins of E. multilocularis (13). These findings prompted us to study AE-DC activation and maturation within the peritoneal cavity of AE-infected mice. Therefore, we determined the gene expression levels of selected

cytokines (TGF-β, IL-10 and IL-12) and the expression of surface markers for pe-DCs maturation. As MHC class II (I-a) molecules were weakly expressed, we further investigated the relative gene expression levels of different molecules involved in the newly synthesized MHC class II (I-a) complex and in the formation of MHC class II (I-a)–peptide complexes [class II transactivator factor (CIITA), invariant chain (li), HLA-DM (H-2Ma), class II β-chain (I-aβ) and cathepsin S (Cat-S)] (14). In addition, we verified whether E/S and V/F might

alter MHC class II (I-a) molecules on BMDCs in vitro. The effect of AE-pe-DCs on a Con A-driven Fossariinae proliferation of naïve CD4+ pe-T cells determined whether AE-pe-DCs exhibited more immunosuppressive rather than stimulating properties. If not otherwise stated, all chemical reagents were from Sigma (St Louis, MO, USA) and all media from Gibco BRL (Invitrogen, Carlsbad, CA, USA). Female 6- to 10-week-old C57BL/6 mice were purchased from Charles River GmbH (Germany) and used for secondary infection with E. multilocularis (and as mock-infected control animals). All mice were housed and handled according to the rules of the Swiss regulations for animal experimentation. The parasite used in this study was a cloned E. multilocularis (KF5) isolate maintained by serial passages (vegetative transfer) in C57BL/6 mice (15). Metacestode tissue was obtained from infected mice by aseptic removal from the peritoneal cavity.