, 2007). Acute encephalitis develops check details in about 1–20 cases per 1000 infections, leading to death in 25% of cases and producing serious neurological lesions in 30% (Diagana et al., 2007; Jackson et al., 2007). Infections with Japanese encephalitis virus (JEV) are most often asymptomatic. Only one in 300 cases produce clinical features (Solomon, 1997). The first signs of infection

appear after an incubation period of between 6 and 14 days (Diagana et al., 2007). The disease usually begins with a high fever, chills, muscle pain and meningitis-type headaches accompanied by vomiting. The initial clinical features in children usually involve gastrointestinal symptoms (nausea, vomiting and abdominal pains). These nonspecific symptoms can continue for 2–4 days. After this period, the patient’s condition deteriorates RAD001 mouse rapidly. Eighty-five percent of subjects suffer from convulsions (Kumar et al., 1990). The meningeal syndrome predominates, causing painful neck stiffness. Additionally, motor paralyses including hemiplegia and tetraplegia may also occur. In about 30% of patients, tremor, rigidity, abnormal movements and other signs of extrapyramidal involvement

are present (Kumar et al., 1994). Recovery usually leaves serious behavioral and neurological sequelae such as persistently altered sensorium, extrapyramidal syndrome, epileptic seizures and severe mental retardation in children (Diagana et al., 2007). JE is a mosquito-borne arboviral infection caused by Flavivirus transmitted by anthropophilic rice field-breeding mosquitoes of the Culex species (mainly the Culex tritaeniorhynchus group). Vaccines have reduced the incidence of JE in some countries, but Non-specific serine/threonine protein kinase no specific antiviral therapy is currently available. Sampath & Padmanabhan (2009) pointed out the following molecular targets

for the flavivirus drug discovery: envelope glycoprotein, NS3 protease, NS3 helicase, NS5 methyltransferase and NS5 RNA-dependent RNA polymerase (Fig. 1). The NS3 protein (nonstructural protein 3) of JEV is a multifunctional protein combining protease, helicase, and nucleoside 5′-triphosphatase (NTPase) activities (Sampath & Padmanabhan, 2009). In particular, NS3 helicase/NTPase seems to be a promising antiviral drug target, as its enzymatic activity is essential for viral genome replication, transcription and translation (Yamashita et al., 2008). Recently, the crystal structure of the catalytic domain of JEV NS3 helicase/NTPase has been solved using a roentgenographic method with a resolution of 1.8 Å (Yamashita et al., 2008). JEV helicase, composed of three domains, displays an asymmetric distribution of charges on its surface, and contains a tunnel large enough to accommodate single-stranded RNA. Each of the motifs I (Walker A motif), II (Walker B motif) and VI contribute to the NTP-binding pocket. From mutation analysis (Yamashita et al.

The CD4+ T cells were incubated with magnetic beads conjugated with an anti-CD25 monoclonal selleck kinase inhibitor antibody to separate CD4+ CD25+ and CD4+ CD25− T-cell subpopulations. The purity of the resulting T-cell subpopulations was higher than 95% by flow cytometry. To determine the suppressive capacity of hASC-induced Treg cells, proliferation assays were performed in triplicate by culturing CD4+ CD25− cells (responder, 5 × 104 from splenocytes of EAHL mice), CD4+ CD25+ T cells (suppressor, 5 × 104 from splenocytes of β-tubulin-immunized mice treated with either hASCs or PBS) in 96-well plates with irradiated antigen-presenting cells (5 × 104 from splenocytes

of normal BALB/c mice) for 72 hr at 37° in complete medium. Cultures were stimulated by β-tubulin (10 μg/ml), and some co-cultures were treated with anti-IL-10 antibody (10 μg/ml). After 72 hr, the proliferation of autoreactive T cells was assayed by measuring bromodeoxyuridine-substituted DNA incorporation. Data were analysed using analysis of variance or Student’s t-test to compare differences between the treatment check details groups. In the present study, we investigated the potential therapeutic effect of hASCs in an experimental model of murine autoimmune hearing loss. Mice were examined weekly for ABRs for hearing capacity. After three injections (Fig. 1a), the hASC administration

group showed that the ABR threshold to click stimulus and wide range of specific frequencies, in comparison with the PBS control group, significantly decreased. After six injections of hASCs (Fig. 1b), ABR click

and pure tone thresholds of the hASC administration group showed improved hearing level at all frequencies tested from 8 to 32 kHz. The ABRs detected threshold levels similar to those in naive mice that received no treatment (Fig. 1b), and the hASC administration completely restored hearing in deaf mice, whereas the PBS control group developed EAHL. Therefore, electrophysiology tests demonstrated recovery of hearing to click stimulus and a wide range of specific frequencies after six injections of hASCs. We investigated the possible immune-modulating effect of hASCs on T-cell priming and differentiation in vivo by examining the recall NADPH-cytochrome-c2 reductase response to β-tubulin in isolated splenocytes from hASC-treated or PBS-treated mice with EAHL in vitro. To determine the ability of hASC treatment to suppress the ongoing inflammatory process, mice with EAHL were treated with PBS or hASCs once a week for 6 consecutive weeks after β-tubulin immunization, and splenocytes that were isolated 10 days after the last treatment with the hASCs were assessed for proliferative responses to β-tubulin. T cells from hASC-treated mice exhibited a significantly decreased stimulation index compared with that in cells from PBS-treated mice (Fig. 2a). Moreover, T cells from hASC-treated non-immunized mice did not develop a xenogenic response to the hASCs in those non-immunized animals (data not shown).

The combination of CpG ODN with cGAMP is a potent type 1 adjuvant, capable of inducing strong Th1 type responses, as demonstrated by enhanced antigen-specific IgG2c and IFN-γ production, as well as cytotoxic CD8+ T-cell responses.

In our murine tumor models, intra-tumoral injection of CpG ODN and cGAMP together reduced tumor size significantly compared with the singular treatments, acting as an antigen-free anti-cancer agent. Thus, the combination of CpG ODN and a STING ligand may offer therapeutic application as a potent type II IFN inducer. This article is protected by copyright. All rights reserved “
“Cholestasis can cause translocation of gut bacteria, and endotoxemia, and systemic inflammation. Now, little is known about the effects of cholestasis on the testicular inflammation and autophagy. A rat biliary cholestasis model caused by common bile duct ligation (CBDL), together with biliary decompression (choledochoduodenostomy), was selleck kinase inhibitor used. The magnitude of MCP-1 expression and CD68+ macrophage infiltration within testes was progressively up-regulated in rats Fer-1 concentration along with increasing duration of CBDL and was maintained at relatively high level in rats with biliary decompression. The large up-regulation of testicular ATG-12, LC3II, and autophagic vacuoles was found with the extending duration of

CBDL and kept at 5 weeks following biliary decompression. The autophagic contents were a large accumulation of mitophagy in testes in rats with CBDL, and cytosol Meloxicam components in rats with biliary decompression. Secondary biliary cholestasis can promote inflammatory reaction and the activation of mitophagy and autophagy in testes. “
“The production of allergen-specific IgE antibodies (Abs) in allergen-sensitized patients or animals has a mutual relationship with the immunologic response leading to allergic rhinitis. We recently reported that, after an intranasal injection of cedar pollen into mice, an interleukin-4 (IL-4)-dependent increase in serum nonspecific IgE Abs was a prerequisite for the

production of serum allergen-specific IgE Abs. Here, we explored which lymphoid organs were responsive to the intranasally injected allergen and how IL-4 and IgE Abs were produced in the lymphocytes. Time-dependent changes in the total cell numbers and in in vitro IgE Ab production in various lymphoid organs revealed that the submandibular lymph nodes were the main responsible organ. After treatment with allergen (for IgE production) or allergen and complete Freund’s adjuvant (for IgG production), we separated submandibular lymph node cells into macrophage-, lymphocyte-, and granulocyte-rich populations by discontinuous Percoll density-gradient centrifugation. Unexpectedly, bulk cells, but not the lymphocyte- or macrophage-rich populations, produced significant amounts of IL-4, IgE, and IgG; whereas production was restored by addition of Mac-1+ cells from the macrophage-rich to the lymphocyte-rich fraction.

We report a case of a 64-year-old male who presented with a large sacral Marjolin’s ulcer secondary to recurrent pilonidal cysts and ulcerations. The patient underwent wide local composite resection, which resulted in a wound measuring 450 cm2 with exposed rectum and sacrum. The massive Lorlatinib solubility dmso defect was successfully covered with a free transverse rectus abdominis myocutaneous flap, providing a well-vascularized skin paddle and obviating the need for a latissimus flap with skin graft. The free-TRAM flap proved to be a very robust flap in this situation and would be one of our flaps of choice for similar defects. © 2012 Wiley Periodicals, Inc. Microsurgery, 2012.

“
“Purpose: We have previously described a means to maintain bone allotransplant viability, FK228 cell line without long-term immune modulation, replacing allogenic bone vasculature with autogenous vessels. A rabbit model for whole knee joint transplantation was developed and tested using the same methodology, initially as an autotransplant. Materials/Methods: Knee joints of eight New Zealand White rabbits were elevated on a popliteal vessel pedicle to evaluate limb viability in a nonsurvival study. Ten additional joints were elevated and replaced orthotopically in a fashion identical to

allotransplantation, obviating only microsurgical repairs and immunosuppression. A superficial inferior epigastric facial (SIEF) flap and a saphenous arteriovenous (AV) bundle were introduced into the femur and tibia respectively, generating a neoangiogenic

bone circulation. In allogenic transplantation, Anacetrapib this step maintains viability after cessation of immunosuppression. Sixteen weeks later, X-rays, microangiography, histology, histomorphometry, and biomechanical analysis were performed. Results: Limb viability was preserved in the initial eight animals. Both soft tissue and bone healing occurred in 10 orthotopic transplants. Surgical angiogenesis from the SIEF flap and AV bundle was always present. Bone and joint viability was maintained, with demonstrable new bone formation. Bone strength was less than the opposite side. Arthrosis and joint contractures were frequent. Conclusion: We have developed a rabbit knee joint model and evaluation methods suitable for subsequent studies of whole joint allotransplantation. © 2011 Wiley Periodicals, Inc. Microsurgery, 2012. “
“False aneurysms in the hand are rare. A false aneurysm of the common digital artery in the palm for the second and third finger is reported, illustrating our experience with arterial graft reconstruction after excision as a valid alternative surgical therapy to a vein graft, when ligation or end-to-end anastomosis are not indicated or feasible. The superficial palmar branch of the radial artery was chosen as donor vessel based on the similarity in vessel diameter and wall thickness to the common digital arteries.

Contrary to common belief, a sequential interaction of licensed DCs with CD8+ T cells barely improved CTL expansion. In sharp contrast, simultaneous encounter of Th cells and CTLs with the same DC during the first in vitro encounter is a prerequisite for optimal subsequent CTL https://www.selleckchem.com/products/AZD2281(Olaparib).html expansion in our in vitro system. These data suggest that, in contrast to DC maturation, the activation of DCs by Th cells, which is necessary

for optimal CTL stimulation, is transient. This knowledge has significant implications for the design of new and more effective DC-based vaccination strategies. Furthermore, our in vitro system could be a valuable tool for preclinical immunotherapeutical studies. “
“Trichinella spiralis and Trichinella pseudospiralis exhibit differences in the Luminespib supplier host-parasite relationship such as the inflammatory response in parasitized muscles. Several studies indicate that matrix metalloproteinases (MMPs) represent a marker of inflammation since they regulate inflammation and immunity. The aim of this study was to evaluate the serum levels of gelatinases (MMP-9 and MMP-2) in mice experimentally infected with T. spiralis or T. pseudospiralis, to elucidate the involvement of these molecules during the inflammatory

response to these parasites. Gelatin zymography on SDS polyacrilamide gels was used to assess the serum levels and in situ zymography on muscle histological sections to show the gelatinase-positive cells. In T. spiralis infected mice, the total MMP-9 serum level increased 6 days post-infection whereas, the total MMP-2 serum level increased onward. A similar trend was observed in T. pseudospiralis infected mice but the MMP-9 level was lower than that detected in T. spiralis infected mice. Significant differences were also observed in

MMP-2 levels between the two experimental groups. The number of gelatinase positive cells was higher in T. spiralis than in T. pseudospiralis infected muscles. We conclude that MMP-9 and MMP-2 are markers of the inflammatory response for both T. spiralis and T. pseudospiralis infections. “
“The term ‘neuromyelitis optica’ (‘Devic’s syndrome’, NMO) refers to a syndrome characterized Isotretinoin by optic neuritis and myelitis. In recent years, the condition has raised enormous interest among scientists and clinical neurologists, fuelled by the detection of a specific serum immunoglobulin (Ig)G reactivity (NMO-IgG) in up to 80% of patients with NMO. These autoantibodies were later shown to target aquaporin-4 (AQP4), the most abundant water channel in the central nervous system (CNS). Here we give an up-to-date overview of the clinical and paraclinical features, immunopathogenesis and treatment of NMO.

Nuclei were counterstained with Hoechst (Molecular Probes/Life Technologies, Grand Island, NY, USA). Stained sections were analysed using a fluorescence microscope (Olympus BX51; Olympus). Selleck EGFR inhibitor Fluorescence images were captured using Cell F software (Olympus). Images captured are representative of greater than seven fields of view at ×20 magnification per mouse. Frozen sections (6 μm) were fixed in ice-cold acetone/ethanol

3:1 solution and blocked with blocking buffer [10% serum, 5% fish gelatine, 0·05% Tween-20, 1% bovine serum albumin (BSA), 0·1% sodium azide]. Colon sections were incubated with anti-mouse Ki67 (Biolegend, San Diego, CA, USA) and counterstained with Hoechst (Molecular Probes). Stained sections were mounted with Prolong Gold anti-fade mounting medium (Molecular Probes) and visualized using a fluorescence microscope (Olympus BX51; Olympus). Fluorescence images were captured using Cell F software (Olympus). Images captured are representative of greater than seven fields of view at ×20 magnification per mouse. Frozen distal colon tissue samples were thawed, transferred

to magNALyser green bead tubes (Roche) and homogenized using the magNALyser homogenizer three times for 15 s at 6500 g (Roche). Total protein was isolated by lysing the distal colon tissue in RIPA buffer [150 mM NaCl, 50 mM Tris-Cl, pH 7·4, 1% NP-40, 0·25% sodium deoxycholate, 1 mM Na3VO4, 1 mM ethylenediamine tetraacetic acid (EDTA)] supplemented with a protease and phosphatase inhibitor cocktail (Sigma). Total protein was resolved by sodium dodcyl sulphate-polyacrylamide X-396 mw gel electrophoresis (SDS-PAGE) gels, transferred to polyvinylidene difluoride (PVDF) membrane and immune blotted for cleaved caspase-3 (Cell 6-phosphogluconolactonase Signalling, Boston, MA, USA), and β-actin (Sigma). Statistical analysis was determined using

one-way analysis of variance (anova)/two-way anova with post-hoc analysis (Tukey’s post-hoc test and Bonferroni’s post-hoc test). qRT–PCR expression data were calculated using the 2-ΔΔCT followed by unpaired t-test and Mann–Whitney t-test to compare differences between groups. Statistical analysis was performed using GraphPad software (San Diego, CA, USA). Data are represented by mean ± standard error of the mean with P < 0·05 considered statistically significant. To assess the role of Bcl-3 in inflammatory bowel disease we initially analysed the Bcl-3 expression levels from a previously published study which identified a large number of genes associated with inflammatory bowel diseases [21]. In that study, transcriptional profiles were generated from biopsies taken from the sigmoid colon of patients with CD (n = 10) and UC (n = 10) and those of normal controls (n = 11). Our bioinformatics analysis of this data set revealed that Bcl-3 mRNA expression levels were increased significantly in both CD (P < 0·01) and UC (P < 0·05) (Supporting Information, Fig. S1).

Recent literature reports can, at least partially, endorse this interpretation. For example, Espinoza-Jiménez et al. (23) found no enhancement in the amount of regulatory T cells during murine Taenia crassiceps infection. In addition, it has been demonstrated that parasite survival in the host depends upon the elicitation of different adaptative immune responses (24). The contribution of regulatory T cells to this complex parasite/host interaction was recently investigated. D’Elia et al. (25) revealed a role for regulatory T cell in the control of Trichuris-induced gut pathology and, moreover, suggested that the helminth uses this cell subset to promote its

own survival within the host. Still in this context, it is important to highlight that there is

an enormous amount of data Doxorubicin on the ability of Schistosoma sps, which cause chronic diseases, Selleck Pirfenidone to determine the suppression of experimental immunological disorders (26). This downmodulatory ability of Schistosoma mansoni has been clearly demonstrated in the CNS inflammation (27,28). Even in the absence of regulatory T cells, Th2 polarization could still provide an environment capable of modifying EAE development as has been reported for diabetes (29) and arthritis (30). To test this possibility, fifteen days after last S. venezuelensis inoculation, experimental encephalomyelitis was induced by inoculation of myelin emulsified with CFA. Contrary to the hygiene hypothesis, the clinical evolution of this neurological disease was very similar in the two experimental groups, i.e., noninfected and previously infected with S. venezuelensis. They equally lost weight, the average clinical score was the same and acute and remission phases also occurred at comparable time periods. This was confirmed by further histopathological evaluation, whose quantitative analysis of the inflammatory infiltrates indicated similar values at the brain and lumbar spinal cord, independently of a previous contact with the helminth. These findings were unexpected and

different from many reports that characterized the ability of helminth infections to protect against new diabetes (31), arthritis (32) and also EAE (33). Only a few articles emphasized this lack of helminth immunomodulation on allergic diseases (34,35). A chronological dependence upon the helminth infection could explain this finding. For example, Wohllenben et al. (36) found a decrease in allergen-induced airway eosinophilia and eotaxin levels in the airways when mice were infected 4 weeks but not 1 or 2 weeks before allergen airway challenge. In spite of this absence of protection, we believe that these findings will contribute to elucidate the limits of the hygiene hypothesis. In this sense, a comparative investigation employing different helminth spp.

In the medical assessment of the potential donor, a critical estimation is made of their future risk of kidney failure and cardiovascular disease. If the risk is predicted to be too great then the living kidney donation should not proceed. There is no direct evidence quantifying the outcome of patients with impaired glucose tolerance who proceed to donate a kidney for transplantation. This is primarily related to the traditional practice of not using patients with diabetes mellitus or impaired glucose tolerance as living kidney donors. Many of these recommendations are extrapolated from the documented natural history

of patients with impaired glucose tolerance. The following definitions of impaired glucose tolerance have been proposed:1,2 A fasting plasma glucose on two occasions of 7 mmol/L indicates diabetes mellitus 6.1–6.9 mmol/L indicates impaired fasting glucose <6.1 is normal FDA approved Drug Library A standard 2 h OGTT with a 2 h glucose concentration of 11.1 mmol/L indicates diabetes mellitus 7.8–11.0 mmol/L indicates

impaired glucose tolerance <7.8 mmol/L is normal. The presence of diabetes mellitus is a contraindication for living kidney donation due to the 25–51% long-term risk of the individual developing diabetic nephropathy.3,4 Despite the common practice of avoiding people with diabetes mellitus and impaired glucose tolerance as living selleck kinase inhibitor kidney donors, the development of type 2 diabetes mellitus in living kidney donors is documented. Due to the lack of suitable controls, however, it is unclear if this is at an increased

rate compared with normal ageing. In the event that diabetic nephropathy does develop, the reduced renal reserve in a donor will MYO10 lead to a more rapid onset of end-stage kidney disease. Chronic kidney disease does increase the risk of cardiovascular events and all cause mortality.5 It is unclear if a similar increased risk is associated with chronic kidney disease that has resulted from donor nephrectomy, although a rise in blood pressure seems to occur.6 Concern would be raised as to the possibility that the chronic kidney disease that results from donor nephrectomy may have an additive or synergistic effect with impaired glucose tolerance or diabetes to increase the cardiovascular risk, adding further weight to avoiding the use of diabetics as living kidney donors. Patients with impaired glucose tolerance have a 5-year risk of developing type 2 diabetes mellitus of 30% if they have a family history of type 2 diabetes (parent or sibling) and 10% if there is no family history.7 This risk may be higher with certain ethnic groups (e.g. ATSI, South East Asians).8 In addition, impaired glucose tolerance induces an increased risk of cardiovascular events even in the absence of overt diabetes mellitus, especially in the context of the metabolic syndrome.

Consequently, the use of this one peptide for stimulation of specific cells would be expected to detect the majority of Gag-specific CD8+ T cells in this mouse strain. Independent of the route and number of immunizations, T cells isolated from different tissues preferentially produced IFN-γ; significant numbers of IL-2-producing cells could not be detected (>55 spot-forming units (SFU)/106 lymphocytes).

Examples for the results are shown in Fig. 2B, which presents data from mice immunized 2 wk earlier i.n. or i.m. with AdC6gag. Similar results were obtained at later time points or after prime-boost regimens (data not shown). Numbers of IFN-γ-secreting cells were higher in spleen, blood, ILN and the GT upon i.m. immunization (p<0.05). Although samples RG7420 from the GT showed secretion of IFN-γ in response to the antigen, we had expected higher SFU numbers from this compartment based on the SFU numbers obtained by tetramer staining (higher in GT than in blood or spleen (p<0.05) for both i.n. and i.m administration). However, ELISpot assays showed

significantly higher secretion of IFN-γ in blood than in GT for the i.n. group (p<0.05) and comparable numbers for the i.m.-primed mice. It is feasible that cells from the GT or NALT secrete cytokines other than IFN-γ or IL-2 and therefore BI-2536 escaped detection by the ELISpot assays. Although this was not ruled out, we favor the explanation that vaccine-induced T cells from the GT and NALT are comparatively frail and thus more readily detected by staining procedures that do not require lengthy incubations. In order to further address this issue, mice were immunized with AdC6gag i.m. and tetramer frequencies were Megestrol Acetate evaluated from cells isolated from the GT either directly without further culture, or after an overnight culture at 37°C with or without the specific peptide. Cells were stained with an Ab to CD8α, the specific tetramer,

a live cell dye and analyzed by flow cytometry. We observed pronounced cell death after overnight incubation of cells especially upon stimulation with the specific peptide; accordingly numbers of tet+CD8+ T cells declined ∼25- or 150-fold upon overnight in vitro culture in medium or the Gag peptide, respectively (data not shown). To elucidate potential differences between T cells isolated from distinct compartments, expression levels of CD44, CD27 (two lymphocyte activation markers), CD62L, an LN homing marker differentially expressed by effector and central memory cells, and α4β7, an integrin that favors migration to the gut mucosa, were determined on tet+CD8+ T cells induced by AdC6gag. Figure 3A shows data for naïve CD8+ lymphocytes compared with tet+CD8+ T cells 4 and 10 wk after a single i.n.

The exact composition of tolerosomes is not known, but it is thought that they may contain other co-stimulatory molecules, which may induce tolerance to the MHC-associated peptide (42). The discovery of tolerosomes is relatively recent, having occurred less than 10 years ago. It has been known since 1983 that, in order for oral tolerance to develop, an intact portal circulation

is needed, and that oral tolerance is transferrable through serum. These cell fragments, the so-called tolerosomes, first discovered by electron microscopy in 2001, were found in the insoluble fraction produced by ultracentrifugation from the serum of animals which had been subjected to induction of oral tolerance. The soluble fraction, serum without tolerosomes, was no longer able to mediate the transfer of oral tolerance (41). This proved that intercellular communication occurs through exosomes

during development X-396 supplier of oral tolerance. The fate of tolerosomes after their production has not yet MDX-1106 been fully elucidated. It is supposed that they bind to local or distant antigen presenting cells (43, 44), conveying the necessary information for mounting tolerance to food antigens. In any case, the fact that the portal circulation is involved in this process has lead to the speculation that tolerosomes can be directed to the liver, another recognized tolerogenic site (45, 46). Oral tolerance

has been exploited for therapeutic purposes to inhibit all forms of unwanted immune responses, from the secretion of different antibody classes, to type IV hypersensitivity reactions. It is to be noted that Th1-type responses are much easier to inhibit than Th2 responses. In order to suppress a Th2 immune response, it is necessary to administer greater antigen quantities, or to increase the frequency of administration (47). An exception to this rule is that of IgE-mediated Th2 immune responses associated with increased production of IL-4, such as allergies, Cediranib (AZD2171) which respond very well to oral tolerization schemes (48). The idea of using SEA in order to augment oral tolerance to different peptides arose from epidemiologic studies (49). Staphylococcus aureus is now a common commensal in the gut in the occidental population (50, 51). It has been demonstrated that Western infants with a greater degree of colonization with SEA-producing S. aureus strains are protected against food allergy (52, 53). Toxigenic S. aureus residing in the gut induce greater concentrations of IgA in children’s serum and protect from eczema (54). Animal models of allergic diseases suggest that neonatal oral administration of SEA followed by feeding the sensitizing protein OVA in adulthood prevents the development of airway allergy when the mice are re-exposed to intranasal OVA (35).