Vasopressors were administered at treatment levels for shock. Neither developed flap compromise, suggesting that pharyngeal reconstruction with an ALT flap may be safely performed in the setting of continuous high-dose vasopressors. Acalabrutinib concentration © 2013 Wiley Periodicals, Inc. Microsurgery 34:237–239, 2014. “
“Intestinal malrotation results from failure of intestinal rotation and fixation during fetal life. We report two cases of esophageal reconstruction with free jejunal flaps

following total laryngopharyngectomy of hypopharyngeal and cervical esophageal carcinoma in which intestinal malrotation was detected during the jejunal flap harvesting. In both cases, the ligament of Treitz was absent, and the laparotomy incision was

thus extended to identify the jejunum. In case 1, harvesting an adequate length of the vascular pedicle of the flap was impossible because of the abnormal position of the pancreas; thus, BMN 673 concentration a jejunal flap of maximal length was harvested for optimal pedicle positioning in the recipient site. In case 2, Ladd’s ligament prohibited the release of the jejunum from the ascending colon and required its dissection. Both patients underwent successful reconstruction. When the ligament of Treitz is absent during jejunal flap harvesting, investing the whole bowel by extended laparotomy incision is recommended. When anatomical abnormality caused by intestinal malrotation is detected, releasing an adhesion of the jejunum from circumferential

organs and identifying the adequate vascular pedicle of a jejunal flap are necessary. If harvesting the long vascular pedicle is impossible, a jejunal flap of maximal length should be harvested for optimal positioning for vascular anastomosis at the shortest distance Fludarabine purchase in the recipient site. © 2014 Wiley Periodicals, Inc. Microsurgery 34:582–585, 2014. “
“The conventional method of microvascular anastomosis with interrupted sutures is well proven method, with high successful rate. However, this method is time consuming, especially when multiple anastomosis are required. Even though several techniques have been described to minimize the time of anastomosis, none of these have been widely accepted.[1, 2] Vessel anastomosis with a continuous suture has the advantage of being faster than the conventional method but due to the high risk of stricture at the anastomotic site is not recommended for microvascular anastomosis.[3] Herein, we present a novel method of performing microvascular anastomosis, which combines the advantages of the continuous and interrupted sutures. After proper setup of the vessels, the anastomosis begins with the application of two 10-0 sutures at 0° and 180° angle (Fig. 1A). Then a loose running suture is applied at the anterior wall of the vessel. Depending on the size of the vessel, usually 3 to 4 passes of the suture are required, creating 2 or 3 loops, respectively. (Figs.

35 In a retrospective review of patients commencing dialysis in a metropolitan New York hospital, Ifudu et al. in 1996 reviewed the outcomes of 139 patients who had been commenced on dialysis between January 1990 and December 1994. Patients were stratified according to whether they had received predialysis care from a nephrologist (43% of cohort) or a non-nephrologist physician (45%) or had received no predialysis medical care (12%).36 Patients who had a period of predialysis care by a nephrologist had a significantly reduced need for emergency central venous access (36% vs 69% vs 100%, nephrologist CDK activity vs non-nephrologist vs no care, P = 0.0001) and reduced

length of hospital stay for the initiation of dialysis (12 ± 23 days vs 25 ± 21 vs 29 ± 23 days, respectively, P = 0.002). Patients who had received predialysis care from a nephrologist were characterized by a lower mean serum creatinine and less severe acidosis than the other two groups at the time of commencement of dialysis. Abdulkader et al. looked

at risk factors for hospital death of patients with CKD who were first reviewed by a nephrologist as an emergency in-hospital referral.37 A total of 414 patients were seen in a tertiary hospital in São Paolo in Brazil. Mortality was 13%. Non-survivors were older, required ventilation and inotropic support, had a higher rate of infection and had a lower creatinine (attributed to malnutrition). Avorn et al. identified 3014 patients who started dialysis in a 6-year period and who were known to have renal

disease more than 12 months Ivacaftor manufacturer prior to commencement.38 There was a 37% increased mortality rate at 1 year in those who had not seen a nephrologist until 90 days or less before starting dialysis. Similarly, those who saw a nephrologist 5 times or less in the 12 months preceding dialysis had a 15% higher mortality rate than those seen more than 5 times. Avorn et al., in a similar cohort of 2398 patients with a diagnosis of renal disease at least 1 year before initiation of dialysis, showed that those who had seen a nephrologist more than Unoprostone 90 days prior to starting dialysis were 38% more likely to have undergone predialysis access surgery (OR 1.38, 95% CI: 1.15–1.64).39 Late referral patients were more likely to start dialysis with temporary vascular access (OR 1.42, 95% CI: 1.17–1.71). Cass et al., in an Australian study using ANZDATA, showed that late referral (<3 months) reduces access to transplantation.40 A total of 3310 patients were studied, of whom 892 were referred late. These patients had more comorbidities and were more likely to have diabetic nephropathy. Adjusting for variables including age and comorbid conditions, they had an OR of listing on the transplant list of 0.49 (95% CI: 0.41–0.59) and were less likely to receive a transplant (HR 0.65, 95% CI: 0.55–0.77).

Thus, it is possible that MZ B-cell differentiation is specifically driven by BAFF. In support hereof, we observed a positive correlation between BAFF levels in WT and TCRβ/δ−/− mice, although due to the

small differences in BAFF levels the analysis failed to reach statistical significance (Pearson test: R2 = 0.29, p = 0.22, n = 7, data not shown). Due to the function of Act1 on BAFF responsiveness rather than BAFF production, we were unable to extend this analysis to Act1-deficient mice. Given the many known JAK2 inhibitor drug roles of Act1, Act1-deficient mice develop a complex phenotype involving many cell subsets. Even in B cells, Act1 appears to play multiple roles (i.e. control of CD40 and BAFF-R-signaling and responsiveness to IL-17A). Interestingly, it has been shown that IL-17A functions to increase B-cell survival, proliferation, and differentiation and hence supports the generation and persistence of autoreactive B cells [37]. As Act1 is a positive regulator of IL-17A signaling and a negative regulator of BAFF, it follows phosphatase inhibitor library that the balance of Act1 binding to either IL-17R or BAFF-R is crucial for maintaining B-cell tolerance (Fig. 8). T-cell-deficient Act1-sufficient mice express very little IL-17A (data not shown), increased BAFF, and accelerated B cell

maturation (increased T2/T3, MZ, and FM), slightly elevated levels of anti-nuclear IgM antibodies and elevated deposition of IgM-IC in the kidney glomeruli (Fig. 8, bottom left panel). As expected all IgG and IgA production is abolished in the absence of T-cell help, that is, CD40 ligation (Fig. 8, bottom panels). Act1-deficiency on the other Alanine-glyoxylate transaminase hand results in increased BAFF-mediated signaling driving T1 to T2/T3 B-cell maturation and elevated levels of MZ and FM B cells (Fig. 8, top right panel). We suggest that more self-reactive B cells (low BCR-antigen-binding affinity), which would normally have been deleted due to negative selection, survive, and differentiate as a result of BAFF hyperresponsiveness.

In addition, Act1-deficiency increases CD40L-mediated Ig class switching and the differentiation of IgG-secreting plasma cells hence elevated levels of IgG autoantibodies (Fig. 8, top right panel). Whether lack of IL-17-mediated signaling in the absence of Act1 is counteracting this effect by diminishing B-cell survival is currently unknown. Finally, when combining TCR deficiency with Act1 deficiency (TKO mice) it follows that BAFF-mediated signaling is increased leading to increased levels of T2/T3 immature B cells, MZ and FM B cells including cells with self-reactivity. CD40L-dependent class switching is eliminated by the lack of T cells resulting in elevated levels of IgM-secreting anti-nuclear-specific plasma cells (Fig. 8, bottom right panel). In conclusion, T-cell-deficient B6.

1 μCi/106 cells of Na251CrO4 for 90 min at 37° and, where indicated, were pulsed for 45 min with 10−6 m of the different peptides at 37°. Cells were then washed,

and 4 × 103 cells were used as targets of each CTL at different effector to target ratios. The per cent specific lysis was calculated as 100 × [(c.p.m. sample)−(c.p.m. medium)/(c.p.m. Triton X-100)−(c.p.m. medium)], where c.p.m. represents counts/min. Spontaneous release was always < 20% in all cases. None of the tested peptides affected spontaneous release. Enzyme-linked immunosorbent spot-forming cell assay [ELISPOT; for interferon-γ (IFN-γ)] was carried out using commercially available kits (Becton-Dickinson, Franklin Lakes, NJ) according to the manufacturer’s instructions. Z-VAD-FMK selleck inhibitor In brief, 96-well nitrocellulose plates were coated with 5 μg/ml anti-IFN-γ, and maintained at 4° overnight. The following day the plates were washed four times with PBS and blocked for 2 hr with 10% fetal bovine serum-supplemented RPMI-1640 at 37°. The CTLs were added to the wells (in triplicate) at a ratio of 10 : 1 and incubated

with target cells at 37° for 24 hr. Controls were represented by cells incubated with concanavalin A (Sigma-Aldrich, St Louis, MO; 5 μg/ml) (positive control), or with the medium alone (negative control). Spots were read using an ELISPOT reader (A.EL.VIS GmbH, Hannover, Germany). Results are expressed as net number of spot-forming units/106 cells.15 Surface expression of HLA-ABC molecules was detected by indirect immunofluorescence using anti-human HLA-ABC mouse monoclonal antibody (BD Pharmingen, San Diego, CA). Mean logarithmic fluorescence intensity was determined by FACS analysis (Bryte HS; Bio-Rad, Milan, Italy).13 It has been previously demonstrated that the HPV epitope, derived from the EBNA1 antigen (amino acid 407–417) and presented by HLA-B35 and HLA-B53 alleles of the B5 cross-reactive group, is one of the targets of EBNA1-specific Clomifene CTL responses in healthy EBV-seropositive individuals.20 To identify specific responses to this epitope and to obtain HPV-specific CTL cultures for further evaluation, we investigated the presence of HPV-specific memory CTL responses in a panel of HLA-B35

healthy EBV-seropositive individuals. To this end, PBLs obtained from nine healthy HLA-B35 positive, EBV-seropositive donors (Table 1) were stimulated with the HPV peptide.24 As control, parallel stimulations were performed using the HLA-B35-presented YPL epitope derived from the EBNA3A antigen.5 The specificity of CTL cultures was tested after three stimulations using standard 51Cr-release assays against autologous PHA-blasts, pulsed or not with the relevant synthetic peptide. As shown in Fig. 1, HPV-pulsed PHA blasts were efficiently lysed by representative CTL cultures obtained from donors 5, 6, 7 and 8. Three of these donors also responded to the YPL epitope. Overall, these stimulations yielded HPV-specific CTL responses in six of the nine donors tested (Table 1).

So far, three other inflammasome prototypes have been described: the NALP1

inflammasome, the IL-1β converting enzyme protease-activating factor (IPAF) inflammasome and recently the absent in melanoma 2 (AIM2) inflammasome.6 To date, much attention has focused around the inflammatory properties of ASC; however, recent evidence has highlighted the importance of ASC in adaptive immune responses. Studies using ASC−/− mice have Fostamatinib chemical structure revealed its significance in adaptive immunity in several physiological and pathological situations. It seems that ASC is essential to mount protective T-cell and B-cell immunity against influenza virus infection.7 Expression of ASC on dendritic cells (DCs) has also been described as being critical in T-cell priming and the subsequent induction of both antigen-specific cellular and humoral immunity and on the onset of collagen-induced arthritis.8 Furthermore, ASC has also been strongly linked to modulating joint inflammation

in antigen-induced arthritis by affecting the induction of antigen-specific cellular immunity.9 Finally, ASC has been shown to contribute to disease progression in experimental autoimmune encephalomyelitis.10 However, the cellular and molecular basis behind the importance of ASC in adaptive immunity remains largely unexplored. We have previously described how ASC−/− T cells exhibit impaired proliferative capacity in response to both antigen-specific and non-specific (anti-CD3/CD28) stimulation ex Talazoparib solubility dmso vivo.9 In this study we explored the cellular basis for the influence of ASC on T-cell proliferation and subsequent Rebamipide effector function. ASC−/− mice1 and NALP3−/− mice11 were backcrossed into the C57BL/6 background for at least nine generations and were compared with wild-type (WT) littermates in this study. Mice were bred under conventional, non-specific pathogen-free conditions. Mice between 8 and

12 weeks of age were used for experiments. All experiments were carried out in agreement with Institutional and Swiss regulations. CD3+ T cells were enriched from splenocyte suspensions by negative selection using the EasySep mouse T-cell enrichment kit (StemCell Technologies, Grenoble, France). Splenic CD4+ and CD8+ T-cell fractions were purified using magnetic antibody cell sorting CD4+ and CD8+ MicroBeads, respectively (> 95%) (Miltenyi Biotec, Bergisch Glaabach, Germany). T cells (2 × 105/200 μl per well) were cultured in 96-well plates previously coated with anti-mouse CD3 (2 μg/ml, clone 145-2C11; eBioscience, San Diego, CA) and anti-CD28 (2 μg/ml, clone 37-51; eBioscience). For co-culture experiments, different isolated T-cell fractions were plated in 96-well plates at a 1 : 1 ratio (1 × 105 T cells per fraction in 200 μl).

cerevisiae or those not immunized. Furthermore, oral immunization induced T helper 1-type immune responses mediated via increased serum concentrations of IgG2a and an increase predominantly of IFN-γ-producing cells in their spleens and lamina propria. Our findings suggest that surface-displayed ApxIIA#5-expressed on S. cerevisiae may be a promising candidate for an oral vaccine delivery system for eliciting systemic and mucosal immunity. Saccharomyces cerevisiae, which is typically used in oral vaccines and drugs, is classified as a GRAS organism [1, 2]. Currently, there is great interest in developing mucosal, particularly oral, vaccines, because such vaccines would not only induce locally and

systemically protective immune responses Dasatinib against infectious disease, but would also be safe and convenient to administer. Several oral delivery systems Staurosporine datasheet using live oral vaccines such as a Salmonella typhimurium mutant, Lactobacillus spp., or S. cerevisiae [3-5] have been attempted. Among these delivery systems, the S. cerevisiae yeast expression system has several advantages: high expression levels, ease of scale-up, low cost and the adjuvant potential of yeast cell-wall components such as β-1,3-D-glucan and mannan [6]. Yeast-based expression systems have been developed and successfully used to produce

recombinant proteins [2, 6]. These systems have been employed in pharmaceutical, livestock feed and food industry applications [7]. Recently, the genetic engineering technique of yeast cell-surface acetylcholine display has been used to display heterologous proteins on the surfaces of yeast cells [2, 7-9]. This system could be a good candidate for a live oral vaccine carrier because it stably maintains surface-expressed epitopes with a high density of proteins [8]. Actinobacillus pleuropneumoniae is the causative agent of porcine pleuropneumonia, a highly contagious endemic disease of pigs that results in significant economic losses worldwide [10, 11]. A. pleuropneumoniae can result in various clinical signs ranging from peracute to chronic, infected pigs typically having hemorrhagic, necrotizing pneumonia,

often associated with fibrinous pleuritis [10]. The ApxII toxin, which is believed to be involved in the virulence of A. pleuropneumoniae, has been used as a vaccine protein [12]. The antigenic determinant of ApxIIA (ApxIIA#5) has been shown to induce a strong protective immune response against A. pleuropneumoniae [13]. ApxIIA, expressed in either S. cerevisiae or Nicotiana tabacum, has previously been reported to be capable of inducing protective immune responses against A. pleuropneumoniae in mice [3, 12, 14]. Moreover, surface-displayed expression of ApxIIA#5 on S. cerevisiae has been studied and induction of antigen-specific immune responses and protection against A. pleuropneumoniae in mice assessed [9]. In the present study, we demonstrated that surface-displayed expression of ApxIIA#5 on S.

All conditions were tested in triplicate. Cells were incubated at 37°C and 5% CO2. The efficiency of transduction was confirmed by fluorescence microscopy. A luciferase reporter assay was used as described previously [24, 32] to confirm the ability of the recombinant Tax2 proteins to regulate viral transcription. Cell-free supernatants from Tax-treated PBMCs were harvested at various time-points and assayed for MIP-1α,

MIP-1β and RANTES expression by quantitative enzyme-linked immunosorbent assay (ELISA) (R&D Systems), as described previously [24]. Absorbance values at 490 nm were used to quantify the chemokine levels in

the culture Veliparib supplier supernatants from the standard concentration curve and CC-chemokine protein levels were expressed in picograms per millilitre (pg/ml). To determine the activation of the canonical NF-κB pathway, immunofluorescence studies were performed using Tax-treated-PBMCs for an incubation period of 1 and 2 h. Cells were harvested, washed with phosphate-buffered saline (PBS), fixed and cytocentrifuged onto clean glass slides, then permeabilized with 0·3% Triton X-100 (Sigma) and blocked with 5% normal goat serum (Sigma) for 1 h at room temperature. Phosphorylated p65/RelA was detected with phospho-p65/RelA learn more monoclonal antibodies (mAbs) (diluted at 1:100) followed by FITC-labelled goat anti-rabbit IgG (H + L), F(ab′)2 mAbs (diluted at 1:200) and incubated at dark-room temperature for 1 h. 4′,6-Diamidino-2-phenylindole (DAPI; Sigma) was use to stain the nucleus. Slides were mounted using anti-fade fluorescent mounting Lonafarnib cost media. Jurkat and MoT cells were used as negative and positive controls. Images were acquired with an Olympus BX51 epifluorescence microscope equipped with an Olympus DP-70 controller digital

camera system and applicable computer capture software (Tokyo, Japan). ImageJ software was used to determine the intensity of cell fluorescence and the non-specific background was subtracted to obtain the corrected total cell fluorescence (CTCF) as integrated density – (area of selected cell × mean fluorescence of background readings) [33]. PBMCs (1 × 106/ml) were stimulated with 100 pM of recombinant Tax proteins and cells were harvested at 1 or 2 h. Nuclear extracts were obtained and tested for activation of p65/RelA and p50 subunits using the TransAM NF-κB DNA-binding ELISA kit (Active Motif, Carlsbad, CA, USA). Briefly, 10 μg of each nuclear extract were incubated in 96-well plates containing a consensus (5′-GGGACTTTCC-3′) binding site for NF-κB.

In this cohort, each antigen included was tested

for differential reactivity between patients having had PGD (n = 20) and patients without PGD (n = 19) using Student’s t-test. The baseline clinical characteristics of the two groups were well matched except that there were a higher proportion of female donors in the PGD group than in the group without PGD (see Table 1). At a significance threshold of P < 0·001 (equal to false discovery rate < 0·15), we identified only a single antigen, telomerase-associated protein 1, displaying fourfold increased reactivity in patients with PGD. Comparing changes in IgG reactivity with changes in IgM reactivity Raf activity for each antigen included on the microarray, however, we observed that the lower the P-values for these changes, the more frequently they changed in the same direction, see Supporting Information for Fig. S1. Requiring P < 0·05 for the differential reactivity www.selleckchem.com/products/poziotinib-hm781-36b.html of both IgG and IgM, 16 different

proteins (corresponding to 46 different antigens, because several peptides from the same protein were usually detected), were identified. With these significance thresholds, 17 proteins were identified in all (Table 2). For each protein, the reactivity changes listed are for the most significant antigen identified. Out of the 17 proteins identified in this manner, six proteins (HSPD1, HSP90AA1, IGF1R, PRKCA, TARP, and TP53) were previously found to be differentially reactive in connection with bronchiolitis obliterans syndrome (BOS).8 Two-factor analysis of variance for these proteins, with

PGD and BOS as the factors, still identified all proteins except TP53 (P = 0·11) as displaying significant differences for PGD (P < 0·05), see Table 3 and Supporting Information for Fig. S2. We analysed the known interactions between the 17 proteins that displayed significant differential autoantibody reactivity (Table 2). This allowed us to examine whether the informative antigens formed networks with specific biological functions. Other large-scale data integrative methods have shown that well-defined interaction networks can often be functionally related Non-specific serine/threonine protein kinase to pathological processes and complex diseases.8,17 For 15 of the 17 proteins, interaction data were available, and we identified an interconnected network consisting of 12 proteins, which is significantly more than would be expected by chance (P = 3 × 10−6) as determined by randomly selecting 15 proteins out of the 260 proteins on the array where interaction data are available, recording the largest interconnected network possible to construct from these, and repeating this 107 times. Also shown in Fig. 1 are the results of hypergeometric testing on the gene ontology biological process terms assigned to the proteins in the network.

In keeping with the effects on angiogenesis induced by contact hypersensitivity reactions in mouse ears, VS-I-treated mice revealed significantly reduced oedema formation, resulting from lower plasma leakage and inhibition of inflammation-associated vascular remodelling [66]. Intravital microscopy studies of inflamed ears showed a decrease

in the fraction of rolling leucocytes in VS-I-treated mice [66]. In addition to anti-microbial activity [67] Cgs may play important role in the neuroimmune interaction in relation to inflammatory function. This review will remain focused upon the function of Cgs in inflammatory responses in the gut. Circulating CgA levels, a marker for neuroendocrine tumours including carcinoids, have Gamma-secretase inhibitor recently been found elevated in some patients with IBD [68]. In this context the disease activity and TNF-α levels influence the CgA pattern, which could reflect the neuroendocrine system activation in

response to inflammation [69]. In a recent letter addressed to the aforementioned study, Sidhu and collaborators [70,71] confirmed the observation of Sciolia et al.[69] of an elevated level of CgA Inhibitor Library mouse serum in both IBD and diarrhoea-predominant IBS patients. The unifying hypothesis proposed could be the EC cell hyperplasia producing an elevated serum CgA levels, as reported previously [72]. The differential replication of EC cells in IBS patients could also explain why elevated levels are found only in a proportion of patients, and levels decline with time. Further studies of serial serum CgA measurements in both these conditions would strengthen our understanding of the plausible mechanisms behind these observations. In the context of experimental colitis, intrarectal injection of CAT can decrease the inflammatory markers [73]. Disease activity index, macroscopic and histological scores, as well Mannose-binding protein-associated serine protease as myeloperoxidase

(MPO) activity, were decreased significantly in mice treated with CAT compared to mice that received DSS only. Treatment decreased the onset of clinical disease as assessed by loose stools, weight loss and rectal bleeding. In addition, colonic tissue levels of IL-1β, IL-6 and TNF-α were decreased significantly in mice treated with CAT. Conversely, the biochemically modified fragment had no effect on the severity of colitis. These results support the hypothesis that Cgs-derived peptides modulate intestinal inflammation in a murine model of colitis by acting directly or indirectly on the microbiota and the immune system. Identification of the molecular and cellular mechanisms underlying the protective role of this peptide may lead to a novel therapeutic option in IBD.

These organs were disrupted and filtered through

a nylon mesh, and the cells were adjusted to 2·5 × 106 and then surface-labelled with fluorescein isothiocyanate (FITC) anti-rat CD4 (0·5 μg) and allophycocyanin (APC) anti-rat CD25 (0·25 μg). After this step, a staining for Foxp3 by using the phycoerythrin (PE) anti-mouse/rat Foxp3 Staining Set (eBioscience, San Diego, CA, USA) was performed according to the manufacturer instructions. After incubation with these antibodies, the cells were fixed in paraformaldehyde 1% and analysed with a FACSCanto II (BD Biosciences, Franklin Lakes, NJ, USA) flow cytometer and Flow Jo software (TreeStar, Ashland, OR, USA). EAE was induced by inoculation of 25 μg of myelin basic protein (MBP; Sigma, St Louis, MO, USA) emulsified with complete Freund’s adjuvant (CFA) containing 5 mg/mL of Mycobacterium butyricum, in the hind left footpad. Animals were daily Selleckchem Raf inhibitor evaluated for weight loss and clinical score. Signs of disease were graded as 0 (zero): no disease; 1: loss of tonicity in the distal portion of the tail; 2: total Selleck HM781-36B loss of tail tonicity; 3: hind limb weakness (partial paralysis); 4: complete hind limb paralysis and urinary incontinence and 5: moribund. The presence and amount of brain and spinal cord inflammatory infiltrates were assessed during EAE recovery phase (20 days after immunization) as previously described

(12). IFN-γ and IL-10 production Non-specific serine/threonine protein kinase were also determined at this phase. For this, lymph node (popliteal + inguinal) cells were collected and adjusted to 2·5 × 106 cells/mL in RPMI supplemented with 10% fetal calf serum, 2 mm l-glutamine and 40 mg/L of gentamicin, in the presence of 10 μg/mL of myelin or 5 μg/mL of concanavalin A (ConA; Sigma). Cytokine levels were evaluated by ELISA in culture supernatants collected 72 h later, according to manufacturer’s instructions (R & D Systems, Minneapolis, MN, USA). ELISA sensitivity for IFN-γ and IL-10 was 19 and 31 pg/mL, respectively. Data were expressed as mean ± SD. Comparisons between groups were made by Student’s t-test or one-way anova with post-hoc Holm–Sidak test for

parameters with normal distribution and by Mann–Whitney U-test or Kruskal–Wallis test for parameters with non-normal distribution. Significance level was P < 0·05. Statistical analysis was accomplished with SigmaStat for Windows v 3.5 (Systat Software Inc., Witzenhausen, Hesse, Germany). A high number of EPG was detected 8 days after the first worm inoculation. The amount of eggs decreased by day 13 and was very low at days 20 and 27. No more eggs were detected 34 days after initial infection (Figure 1a). Evaluation of specific antibody levels by ELISA indicated significant production of IgG1 but not IgG2b (Figure 1b). The frequency of cells expressing the regulatory foxp3 marker was determined in spleen and lymph node cells.