This is, to our knowledge, the first study investigating TREC levels in IBD patients. Here we demonstrate equal levels

of TRECs in peripheral blood between IBD patients and healthy controls but increased levels of TRECs in the intestinal mucosa of UC patients, but not CD patients, compared to uninflamed controls. In addition to the increased TREC levels in the colon of UC patients, these patients also demonstrated selleck high frequencies of CD3+CD4+ T cells expressing the adhesion molecule L-selectin (CD62L+) but with low expression of CD45RA. We also demonstrated that age has a low impact on the levels of TRECs in the intestinal mucosa and that disease activity did not affect TREC levels in either peripheral blood or the intestinal mucosa. As no increased extrathymic AZD8055 research buy maturation was found in the intestinal mucosa, this strongly suggests that the increased levels of TRECs in the intestinal mucosa of UC patients reflect recent thymic emigrants (RTE) being recruited directly to the mucosa. Substantial

efforts have been devoted to identify a phenotype for RTE and candidate T cell surface markers exist for chicken (chT1) [19,20] and rats (Thy-1, RT6) [21]. For humans, two markers have recently been proposed: CD31 and CD103, both being present on thymocytes at a late stage of development but being lost quickly after T cell entrance into the periphery. However, although the amount of CD31+ T cells Metalloexopeptidase are reduced with increasing age [22–24], the TREC levels within the CD31+ T cell population are also declined [23], suggesting a certain degree of in vivo turnover of CD31+ T cells with ageing. Thus, we believe that TREC content is at present the most reliable marker for recent thymic emigrants, at least when investigating both CD4+ and CD8+ T lymphocytes in the gut mucosa. TREC quantification

has been used to monitor T lymphocyte ontogeny in patients with multiple sclerosis (MS) [25] and rheumatoid arthritis (RA) [26,27]. In line with our findings in UC patients, both studies reported decreased levels of TREC in peripheral blood lymphocytes from patients, compared to healthy controls [25,27]. However, neither study evaluated TREC levels in the affected tissue, the central nervous system (CNS) and joints, respectively. TREC levels in the intestinal mucosa were generally much lower than in peripheral blood in control subjects. This is consistent with the fact that the gut mucosa predominantly contains memory/effector T lymphocyte populations, in which the TRECs will be diluted due to extensive previous proliferation. When comparing TREC content in the three different IEL fractions obtained during the isolation procedure, we found that the number of individuals with positive TREC levels increased from the first to the third fraction in UC patients.

This is likely to be the result of the thorough sampling of a highly restricted portion of sequence space that is revealed by PCR amplification using a forward primer specific for IGHV6-1. MLN0128 In contrast, the relatively low proportion of clonally related sequences seen in this study suggests that the IgE response, in parasitized individuals, may be highly diverse. The varying proportions of clonally related sequences seen in association with different IgG subclasses may also point to varying levels of diversity in these responses, although analysis is confounded by the unequal numbers of different IgG subclass transcripts obtained from different individuals.

Certainly, the high proportion of clonally related IgG4 sequences suggests a lack of diversity which might be expected if this subclass response was restricted to the minor set of the most persistent antigens. Further insights into the IgE anti-parasite response come from analysis of somatic point mutations, and to better interpret our observations of mutations in IgE sequences, we amplified IgG-associated VDJ gene sequences, using IgG subclass-specific reverse PCR primers. The mean mutation levels seen in these 886 unique IgG sequences varied substantially between subclasses and correlated with the position of the constant region

genes within the constant region gene locus (IgG3 < IgG1 < IgG2 < IgG4). Although unexpected, this is in accord with the reports of low-affinity IgG3 being seen early in a response Ceritinib price [25], and high-affinity IgG4 emerging after long periods of persistent antigen stimulation [28]. These studies are consistent with the concept that B cells only switch to IgG4 after multiple rounds of cell division, during which the VDJ sequences accumulate high numbers of mutations [29]. On the other hand, it does not imply that IgG class-switching progresses inevitably by a series of sequential downstream steps, for cells

may switch to IgG4 both directly from IgM and indirectly via other constant region genes, as is also known to occur in the IgE response [30, 31]. Interestingly, despite IgE also being associated with persistent stimulation, and the IGHE gene being downstream of Fenbendazole the IGHG genes, the level of mutation in IgE sequences was similar to that of IgG1 and IgG2 sequences and was significantly less than that of IgG4 sequences. The average number of mutations seen in the IgE-associated VDJ gene sequences was 23.0, which is substantially higher than we previously reported for IgE sequences from individuals with atopic dermatitis, whose mean mutation counts were 14.7 and 15.7 [13, 27]. Higher counts have been seen in individuals with seasonal rhinitis and allergy to grass pollen [32], with a reported median count of 21. While an average of 19.

IgG concentrations prior to and at the time of rituximab

correlated with nadir IgG. IgG replacement was initiated because of recurrent infection in 12 (4.2%) patients and a lower IgG increased the odds ratio of receiving IgG replacement. IgG replacement therapy decreased the incidence and severity of infections, and recovery of IgG concentrations allowed cessation of IgG replacement in two patients after 4 and 7.5 years of replacement treatment. Conclusions: Monitoring of IgG is recommended for patients receiving rituximab. IgG replacement for sustained hypogammaglobulinaemia with recurrent Ruxolitinib infections appears effective. The IgG treatment course is prolonged in most patients, but IgG recovery is reported. 175 PARENTAL PERSPECTIVES ON THE FINANCIAL IMPACT OF CARING FOR A CHILD WITH CHRONIC KIDNEY DISEASE M MEDWAY1,2, PF 2341066 A TONG1,2, JC CRAIG1,2,

S KIM2, F MACKIE3, S MCTAGGART4, B BARTON5, K HOWARD1, G WILLIAMS1,2, A WALKER6, G WONG1,2 1Sydney School of Public Health, The University of Sydney, Sydney, NSW; 2Centre for Kidney Research, The Children’s Hospital at Westmead, Sydney, NSW; 3Department of Nephrology, Sydney Children’s Hospital, Sydney, NSW; 4Department of Nephrology, Royal Children’s Hospital, Brisbane, QLD; 5Children’s Hospital Education Research Institute, The Children’s Hospital at Westmead, Sydney, NSW; 6Department of Nephrology, Royal Children’s Hospital, Melbourne, Victoria, Australia Aim: This study aims to describe parental perspectives on the financial impact of caring for a child with CKD. Background: Chronic kidney disease (CKD) can impose a significant social

and financial burden on patients and caregivers, however little is known about how caregivers experience and cope with the financial impact of CKD. Methods: Face-to-face semi-structured interviews were conducted with 27 parents of children with CKD across three centres in New South Wales and Queensland. Transcripts were thematically analysed. Results: We identified five themes: loss of freedom (prioritizing demands of care, limiting occupational opportunities, appreciating socio-economic advantage); burden of sole responsibility (inability to rely oxyclozanide on others, lack of respite, increased separation of family roles, self-reliance); adapting for survival (vigilant budgeting, redefining normality and expectations, rechanneling resources to basic needs, exploring new income sources, negotiating work flexibility); instability of circumstances (depleted capacity to work, unpredictability of child’s health, burden of travel-related costs, imposition of debt, domestic upheaval); and struggle in seeking support (‘falling through the cracks’, unmet information needs). Conclusions: Parents experienced meeting the complex needs of their child with CKD as an overwhelming focus, which they believed consumed much of their resources, time and energy.

Denervated muscle fibres of sALS and NMA cases and SOD1 mice showed diffusely increased STIM1 immunoreactivity along with ubiquitinated material. In addition,

distinct focal accumulations of STIM1 were observed in target structures within denervated fibres of BYL719 price sALS and other NMA as well as SOD1 mouse muscles. Large STIM1-immunoreactive structures were found in ALS-8 patient muscle harbouring the P56S mutation in the ER protein VAPB. These findings suggest that STIM1 is involved in several ways in the reaction of muscle fibres to denervation, probably reflecting alterations in calcium homeostasis in denervated muscle fibres. “
“In this case report, for the first time, we provide descriptive cliniconeuropathological features of a case of familial amyotrophic lateral sclerosis (familial ALS, FALS) with p.N352S mutation in TARDBP. The present Japanese patient (Figure 1, II-4, the proband) was born in Wakayama Prefecture. At 74 years, he experienced weakness in the muscles of both hand. He visited our neurology department Alectinib in vitro with complaints of impaired fine motor skills of both hands at 76 years, and his neurological examination showed muscle weakness and muscular atrophy of both hands. At 77 years, his muscle weakness descended to both thighs, leading to difficulty

in walking by himself. While his tongue revealed slight atrophy and fasciculation, there were no

detectable upper Decitabine ic50 motor neurone (UMN) signs, cognitive impairment, dysphagia, dysarthria, sensory disturbances, or gait disturbances. Electromyography disclosed active denervation of muscle potentials in both the upper and lower extremities, and he was diagnosed with ALS. His respiratory function gradually worsened, and he died of respiratory failure at 78 years, 4 years after onset. In the patient’s pedigree, his niece (III-2), who is now 60 years old, was also affected by ALS. She had complaints of muscle weakness of the lower extremities at 45 years and is currently on ventilatory support. She can still communicate using lip movements. Informed consent for the gene study was obtained from the patient and his family. Genomic DNA was extracted from peripheral blood leucocytes using standard methods. All exons and exon–intron boundaries of copper/zinc superoxide dismutase (SOD1) and TARDBP were analysed by polymerase chain reaction and direct sequencing, as previously reported [1,2]. TARDBP analysis identified a c.1055A>G heterozygous missense mutation at codon 352 (p.N352S) and no mutation of SOD1. The present study was approved by the ethics committees of all participating institutions. Neuropathologically, brain weight after fixation was 1295 g. Macroscopically, both the cerebrum and cerebellum were preserved. In the brainstem, medullary pyramid volumes were slightly decreased.

Co-stimulation is not only relevant for the generation of effector T cell responses; several co-stimulatory molecules, including CD134 (OX-40), CTLA-4 and ICOS, have been indicated to also contribute to tolerance mechanisms mediated by Tregs[24,25]. CD137 expression has been found on Tregs and CD137 signalling has been shown to promote proliferation and survival of Tregsin vitro[26,27]. In a murine model of diabetes, treatment with anti-CD137 mAb increased Treg numbers significantly, which

mediated protective effects after adoptive transfer into non-obese diabetic–severe Veliparib combined immunodeficiency (NOD–SCID) recipients [17]. In contrast, other studies have pointed towards a negative effect of CD137 stimulation on Treg induction or activity. Choi

et al. demonstrated that CD137 signalling neutralizes the suppressive function of Tregsin vitro and in vivo[43]. Another study suggests that CD137 signalling is not important for Treg function, as Tregs isolated from CD137−/− mice prevented colitis pathology efficiently in a CD4+ T cell transfer model to SCID mice [44]. So far, the exact importance of the CD137/CD137L pathway for Treg function or generation of respiratory tolerance in vivo has not been studied. Therefore, we also investigated whether CD137 might play an immune regulatory role in vivo. CD137 deficiency had no impact on respiratory tolerance induction in our model, as CD137−/− mice were protected equally from the development of allergic parameters FK506 compared to WT mice by mucosal antigen application prior to sensitization. We could not detect changes in Treg frequencies between WT and CD137−/− mice. Thus, the lack

of CD137 seems not to inhibit Treg development or function in our model. Taken together, our results demonstrate that loss of CD137/CD137L signalling neither affects the generation of Th2-mediated allergic airway inflammation nor influences the induction of respiratory tolerance Lonafarnib molecular weight in our murine model. While the current study investigated the role of CD137 in a murine model of allergic asthma, there are only limited data on CD137 function in the human system with regard to allergic, Th2-mediated immune responses: CD137 expression has been detected on eosinophils and associated with apoptosis of eosinophils [45]. Moreover, CD137 expression has been reported on T cells infiltrating the conjunctival stroma in patients with severe allergic conjunctivitis compared with controls [46]. Thus, future studies are required to elucidate the exact role of CD137 signalling in allergic diseases in humans. This study was supported by the German Research Foundation [Research Training Group GRK 1441 ‘Allergic response in lung and skin’; SFB 578 (TP14) ‘Immune reactions of the lung in infection and allergy’].

DC viability and Brucella numbers were analyzed at 1, 4 and 24 h. These data showed that at 4 h, there were relatively similar levels of Brucella : BMDCs. Data were from one of three replicates and

the counts denoted the number of intracellular Brucella per 100 cells. For the 1 : 100 MOI at 1 h, Brucella : BMDCs selleck chemicals for strain RB51 were 35 254 and strain 2308, 4535. For 4 h, Brucella : BMDCs for strain RB51 was 6330 and strain 2308, 19 420; at 24 h, Brucella : BMDCs for strain RB51 was 124 and strain 2308, 2125. These data substantiated that our model allowed both rough and smooth Brucella strains to infect and stimulate BMDCs. Thus, increased activation associated with increased numbers of rough strains appeared to be unlikely. The results reflected the effects of strain differences on BMDC function. Collectively, both data from Surendran et al. (2010) and the data presented here BGJ398 showed that regardless of the viability, the rough vaccine strain RB51 induced enhanced DC maturation compared with the smooth virulent strain 2308. Additionally, the live strain RB51 induced DC maturation and function greater than its respective HK or

IR strain. Furthermore, at MOI 1 : 100, the live strain 2308 induced almost equal or greater expression of DC maturation markers as that of HK or IRRB51 at the same dose. However, none of the smooth strains, regardless of the viability or the dose, induced DC function based on cytokine production. Based on these data, the live strain RB51 provided optimal DC activation and function based on upregulation of MHC class II, CD40, CD86 and Adenosine TNF-α and IL-12 production compared with media control (Figs 1 and 2).

At MOI 1 : 100, the IR and HK strains significantly upregulated MHC class II and CD86 greater than the media; however, neither CD40 expression nor cytokine production was greater than the media. Additionally, at MOI 1 : 100, IR strain RB51 induced significantly less MHC class II and CD86 expression than live strain RB51. These data all supported that live strain RB51 upregulated DC function significantly better than HK or IR strains of RB51. However, the question remains as to whether nonlive Brucella strains can protect against challenge and thus be used as alternative ‘safe’ strains for humans and animals. Additionally, as Brucella has been used as an adjuvant (Golding et al., 1995), the effect of viability on DC function, T-cell function and overall protection is a concern. HK Brucella is an established adjuvant and carrier that promotes a Th1-protective immune response (Finkelman et al., 1988; Street et al., 1990). IR strain RB51 has been shown to stimulate antigen-specific Th1 immune responses (Oliveira et al., 1994; Sanakkayala et al., 2005). In order to generate a strong Th1 response, enhanced DC activation with associated IL-12 secretion is critical (Golding et al., 2001). As DCs are a major source of IL-12 and an important cellular target for Brucella infection (Huang et al., 2001; Billard et al.

ODNs were purchased from Hokkaido System Science (Hokkaido, Japan). The sequences of ODNs were 5′-TCCATGACGTTCCTGATGCT-3′ (CpG ODN1668), 5′-TCCATGAGCTTCCTGATGCT-3′ (non-CpG ODN1720), 5′-gggggACGATCGTCgggggG-3′ (A-type ODN2216), 5′-TCGTCGTTTTGTCGTTTTGTCGTT-3′ (CpG ODN2006), 5′-TGCTGCTTTTGTGCTTTTGTGCTT-3′ (GpC ODN2006) and 5′-TCGACGTTTTGACGTTTTGACGTTTT-3′ (26-mer CpG ODN). Capital letter means PO bond and lower-case

letter means PS bond. B-type ODN1668 has the same sequence as CpG ODN1668 and all bonds of it were substituted by PS bonds. ODN1668 fluorescently labeled by Alexa488 was purchased from FK228 Nihon Bioservice Laboratories (Saitama, Japan). All deoxynucleosides, dNMPs and dNTPs were purchased from Sigma. Plasmid vector pCMV-Luc, a CpG motif replete circular double-stranded DNA, was constructed as previously reported 44. pCMV-Luc has 33 Pur-Pur-CpG-Pyr-Pyr sequences including two GACGTT, a most potent CpG motif for mice 45. pCpG-ΔLuc, another plasmid with no CpG motifs, was constructed as previously reported 46. The plasmid DNA (pDNA)/LA2000

complex was prepared at a ratio of 2 μL LA2000 and 1 μg pDNA according SCH727965 solubility dmso to the manufacturer’s instructions. ODN1720 or pDNA was treated with DNase I or DNase II to prepare degraded DNA samples according to the manufacturers’ protocols of the enzymes. In brief, 1 μg DNA was incubated with 0.5 units DNase I or DNase II at 37°C overnight, and the DNA solution was incubated at 80°C for 10 min to inactivate the DNase in the DNA solution. The degradation of DNA was confirmed by 1% agarose gel electrophoresis (pDNA) or 21% PAGE (ODN). All degraded DNA samples were not detected, indicating sufficient degradation of DNA by DNases. Separately, DNase I-treated ODN1720 and ODNs Vildagliptin with a variety of length were run on a 21% non-denaturing PAGE and stained with CYBR Gold (Invitrogen) as shown in Supporting Information Fig. 4. ODNs with 4 nucleotides or longer were

stained with CYBR Gold, but ODN with a length of 2 nucleotides was not. No bands were observed with DNase I-treated ODN1720, suggesting that the DNase I-treated ODN1720 was ODNs with less than 4 nucleotides. DNase I-treated DNA was treated with alkaline phosphatase according to the manufacturers’ protocols of the enzyme. In brief, 1 μg DNase I-treated DNA was incubated with 0.013 units alkaline phosphatase at 37°C overnight. Then, the phosphatase was inactivated by the addition of 1 μmol EGTA followed by an incubation at 65°C for 10 min. To minimize the activation of cells by contaminated LPS, pDNA samples were extensively purified with Triton X-114, a nonionic detergent, before use according to a previously published method 47. The level of contaminated LPS was checked by a Limulus amebocyte lysate assay using the Limulus F Single Test kit (Wako Pure Chemical, Osaka, Japan).

Splenocytes were removed from both CatG-deficient mice and C57BL6 control mice, and cell surface and total expression of MHC II (I-Ab) was analysed by flow cytometry. Levels of surface (Fig. 6d) or total (not shown) I-Ab in B cells, DCs, and resting or activated buy CHIR-99021 macrophages did not differ between CatG-deficient and control mice. Analysis of peritoneal macrophages also revealed no differences in

I-Ab expression between CatG−/− and C57BL6 control mice (data not shown). We concluded that, by several criteria, CatG lacks the ability to modulate steady-state MHC II levels in vivo and in live, cultured APCs. Our findings provide information on the mechanisms by which MHC II molecules resist endosomal proteolysis, a key biochemical requirement for their function in presentation of peptides captured in endocytic compartments. In their native conformation, purified, detergent-solubilized MHC II molecules failed to be degraded by most lysosomal proteases tested (cathepsins D, L, S, H, and B). The resistance of MHC II molecules to these

proteases thus is an inherent property Alvelestat order of the folded MHC II ectodomains. In contrast, purified MHC II molecules were susceptible to proteolytic attack by CatG at a single cleavage site, which is broadly, but not universally, conserved amongst MHC II molecules. However, using several independent approaches, we were unable to detect any involvement of CatG in the turnover of MHC II molecules embedded in membranes of live APCs. These results

show, on the one hand, that proteolytic resistance of MHC II molecules is not absolute, allowing some scope for regulated turnover; on the other hand, they suggest that the CatG cleavage site is inaccessible in the membrane-embedded native MHC II protein, in vivo. The resistance of MHC II molecules to many endosomal proteases is structurally plausible: the immunoglobulin superfamily domain fold, which is adopted by the membrane-proximal domains, is well known to be highly protease-resistant, and the peptide-loaded antigen-binding groove is highly compact. Initiation of HLA-DR proteolysis by CatG in vitro involved site-specific cleavage between leucine (L) and glutamine (Q) within fx1 and fx2 of the lower loop of the β domain, Nintedanib (BIBF 1120) which may be one of very few sites with sufficient flexibility to allow proteolytic attack. These findings are reminiscent of previous studies, in which CatG was demonstrated to initiate cleavage within the flexible hinge regions of immunoglobulins.39 The membrane-proximal location of the cleavage site, away from the antigen binding groove, is consistent with our observation that CatG cleaves peptide-loaded MHC II molecules, and that peptide binding is retained by CatG-cleaved DR molecules. The fact that peptide-loaded molecules are substrates for CatG supports the notion that CatG is capable of initiating proteolysis of MHC II molecules in their native conformation.

In addition to stimulating factors such as cytokines which can provoke NK cells function, it should be noted that viral infections check details may be as other potent

stimulators of NK cells in AD. It has been shown that CNS infections by herpes simplex virus type 1, picornavirus, Borna disease virus, and other microorganisms such as Chlamydia pneumonia, Helicobacter pylori, and spirochaete could be possible aetiological agents in the development of AD [62, 63]. AD is a progressive and neurodegenerative disorder that accounts for 50–60% of all dementia patients. It is characterized by language difficulties, impairments in decision-making and cognitive dysfunction. The responsible mechanisms in degeneration of cerebral neurons and synapses in AD remain an enigma.

The AD patients’ brain shows some degree of cerebral atrophy, but the extent of neuronal loss varies among patients. The Beta amyloid has been found outside senile plaques and within cerebral blood vessels in AD cases [64]. Increased production of cytokines, such as IL-1α, IL-1β, IL-2, IL-3, IL-6, and TNF-α in senile plaques in the hippocampus and cortex of Alzheimer’s brain has been reported [3]. NK cells are granular lymphocytes that have cytotoxic activities. They can affect adaptive immune responses DNA Damage inhibitor and control immune cell homoeostasis in humans medroxyprogesterone and they can produce cytokines, such as IFN-γ, IL-3, IL-5, IL-10, IL-12 and IL-13 [13]. Recent findings show that NK cells are involved in AD and could be a target for evaluating the immunopathogenesis of this disease and/or approaching to prevention and treatment of AD [9]. Regarding the results of various studies, it seems that although the frequency of NK cells in AD is not affected, however, their functional potential shows some degree of defects [7, 32]. Surprisingly, it has been shown that this anergic behaviour of NK cells in AD patients is not permanent and their NK cells

can be a potent cytotoxic and cytokine secreting cells following cytokine-mediated stimulation [7]. The cause of this behaviour is unknown but it is suggested that dysregulation in signalling pathways is in part involved in this fashion [27]. The precise role of NK cells as protective or deleterious factors in AD immunopathogenesis is also matter of debate. However, knowing this matter that NK cells can be as a therapeutic target in AD therapy requires to more investigation in both human and its animal experimental models in the future. “
“During the past decade, it has been firmly established that IL-23 is essential for disease development in several models of autoimmune disease, including psoriatic skin inflammation, inflammatory bowel disease (IBD), and experimental autoimmune encephalomyelitis (EAE).

5b). There is evidence

that Schistosoma sp. infection protects humans [11] and Everolimus mice against allergic asthma [36,38,40]. We evaluated whether the S. mansoni antigens Sm22·6, PIII and Sm29 could down-modulate the inflammatory allergic response in a murine model of OVA-induced airway inflammation. We found that immunization with these S. mansoni antigens protected mice against allergic inflammation; there was a strong reduction in the number of inflammatory cells and eosinophils recruited to the airways. Moreover, the levels of OVA-specific IgE production were also decreased in mice immunized with Sm22·6, PIII and Sm29, and the levels of EPO in the lungs were lower in mice immunized with Sm22·6 and PIII, compared to the non-immunized mice. Additionally, we found that these two antigens have an important immunomodulatory effect on the production of the Th2 cytokines IL-4 and IL-5, evidenced by the lower levels of these cytokines in the BAL of immunized compared to non-immunized mice. IL-5 is a well-known cytokine that induces the production of eosinophils and activates these cells, while IL-4 acts on B cells, inducing

IgE synthesis. This antibody participates in the pathogenesis of asthma by binding to mast cells, basophils and eosinophils, which release inflammatory mediators upon contact with the allergen. We observed lower levels of allergen-specific IgE in the groups of S. mansoni antigen-immunized mice compared to non-immunized mice. This is additional evidence that these antigens are able to prevent Th2-mediated inflammation. In mice

immunized Wnt beta-catenin pathway with Sm29, despite the fact that there was a reduction in the number selleck compound of inflammatory cells, eosinophils and OVA-specific IgE compared to non-immunized mice, the decrease in the levels of IL-4 and IL-5 in BAL did not reach statistical significance. The slight decrease in IL-4 and IL-5 production might be effective to reduce IgE production and eosinophils growth or recruitment without, however, being sufficient to alter EPO activity in lung tissue. We used the antigen IPSE as our positive control as this antigen is an inducer of the Th2 response in schistosomiasis [34]. As expected, in mice immunized with IPSE the Th2 parameters such as number of eosinophils, levels of EPO, IL-4 and IL-5 were comparable to asthmatic non-immunized mice; unpredictably, however, in IPSE-immunized mice there was a reduction in the levels of OVA-specific IgE. This study examined inflammatory mediators responsible for lung airway inflammation in a murine model of OVA-induced allergic asthma, and found an eosinophil infiltration of the airway. Eosinophils play a pivotal role in the airway inflammation in asthma and they correlate with the extent of inflammatory process in the lung parenchyma [41]. Lung function could not be evaluated in the present study.