6 Cystatin-C is particularly sensitive at detecting changes in kidney function when renal impairment is mild,7 and is better than creatinine for assessment of acute kidney injury due to its shorter half-life.8 Some other potential biomarkers of renal function are also worthy of note. Uric acid is normally excreted through the kidney but circulating levels increase during Fulvestrant molecular weight renal impairment in CKD. Animal model studies have shown that hyperuricaemia activates the renin-angiotensin

system, induces oxidative stress and reduces renal function.9 Increased levels of serum uric acid have been detected in patients with CKD by colorimetric assay and predict a greater risk of end-stage renal disease.9 Urinary levels of angiotensinogen detected by ELISA have been reported to be a specific index of the intrarenal renin-angiotensin system and correlate with blood pressure and glomerular filtration rate in CKD.10 Therefore, urine angiotensinogen appears to be a potential biomarker of renal function in kidney diseases that are dependent on hypertension.

The fractional excretion of magnesium (FE Mg) is considered to be a measure of tubular function because tubules normally reabsorb magnesium filtered by glomeruli.11 Levels of magnesium can be measured in serum and urine by atomic absorption spectroscopy. Elevations in the FE Mg are thought to indicate the loss of peritubular capillary flow resulting from tubulointerstitial damage.11 Oxidative stress is known to play a pathological role in animal models of CKD.12 Increased oxidative stress is AZD5363 ic50 also present in patients with moderate to severe CKD;13 however, further longitudinal and intervention studies are required to help define the role of oxidative stress in the development of human

CKD. Some serum and urine biomarkers have been shown to reliably measure the level of renal oxidative stress in patients and animal models. During oxidative stress, oxidized guanine in cellular DNA is spliced out by DNA repair enzymes, releasing a metabolically stable product 8-hydroxy-2-deoxyguanosine (8-OH-dG) into the urine. Increased levels of 8-OH-dG can be detected in urine by ELISA during CKD.14 Peroxidation of lipids also occurs during oxidative stress, resulting in the formation of 8(F2a)-isoprostane Selleck Ponatinib and 4-hydroxy-2-nonenal. Levels of 8-isoprostane and 4-hydroxy-2-nonenal can be measured in serum or urine by ELISA or HPLC and are elevated in CKD.15–17 In addition, renal oxidative stress produces peroxynitrite that nitrates protein tyrosine residues to form stable 3-nitrotyrosine peptides. A recent study has indicated that levels of 3-nitrotyrosine peptides can now be accurately measured in serum or urine using liquid chromatography and mass spectroscopy, which may prove to be useful for assessing both oxidative and nitrosative stress in kidney disease.

[27]. For the toxin-neutralization check details assay, 20 pg/mL of EHEC-derived Stx2 was preincubated with an equal volume of 100-fold diluted sera from mice immunized with mStx2-His or PBS for 1 hr at 37°C. For the in vivo assays, each Stx2-His was serially diluted with PBS and 0.5 mL of each dilution injected

intraperitoneally into at least five female ICR mice (6 weeks of age, Japan SLC, Hamamatsu, Japan). The animals were observed for 1 week and their deaths were recorded. The MLD was calculated from the dilution that killed all animals. Ten micrograms of mStx2-His containing 0.05% (w/v) of aluminum hydroxide (which has been clinically used as an adjuvant) in 0.2 mL of PBS was injected s.c. twice at a 2-week interval into 25 female ICR mice (6 weeks of age). For a control group, PBS containing 0.05% (w/v) of aluminum hydroxide was injected into five mice instead of

mStx2-His. Two weeks after the secondary immunization, the animals were tail bled to determine the specific serum antibody titer by ELISA. The mice immunized with mStx2-His were then divided into three groups that were intraperitoneally challenged with a 10-, 100-, or 1000-fold lethal doses of Stx2-His and their survivability was monitored for 1 week. All animal experiments were conducted according to the Guidelines for the Management of Laboratory Animals at Fujita Health University. Flat-bottom, 96-well plates were coated with 1 μg/100 μL of Stx2-His overnight at 4°C. After washing the plates three times with T-PBS, each well was blocked selleck screening library using 200 μL of S-PBS for 1.5 hr at 37°C. After washing the plates three times, 100 μL of immunized or untreated (normal) mice sera serially diluted with S-PBS was added to the plates and incubated for 1 hr at 37°C. The plates were washed three times and incubated with 100 μL of HRP-conjugated anti-mouse IgG goat Immunoglobulin (Jackson ImmunoResearch, West Grove, PA, USA) for 1 hr at 37°C. After washing the plates,

the wells were reacted with 100 μL of citrate buffer (pH 5.0) containing 0.04% (w/v) o-phenylenediamine and 0.02% (v/v) hydrogen peroxide for 30 min at 37°C. The reaction was stopped by the addition of 100 μL of 1 M H2SO4 and the absorbance measured 3-mercaptopyruvate sulfurtransferase at 492 nm using a microplate reader (Tecan, Mannedorf, Switzerland). The absorbance value for each sample was compared with that of normal serum at the same dilution, and the antibody titer was determined as a reciprocal of the highest dilution with the lowest positive difference of the 1.5 × absorbance value of normal serum subtracted from the 1 × absorbance value of each sample. Cell lysates from transformants were prepared using previously described methods [25]. The sample proteins were resolved on a 15% polyacrylamide gel. The gel was stained with CBB-R250 or electroblotted onto a PVDF membrane using the iBlot gel transfer system (Invitrogen).

However, after infection or treatment with H. polygyrus AgS, F9 or F17, the percentage of apoptotic cells decreased. The percentage of apoptotic CD8+ cells remained

unchanged. Taken together, during infection and after cell activation by TCR and CD28 receptors, H. polygyrus antigens reduced both the proliferation and apoptosis of CD4+cells. Seventeen fractions were separated from the somatic homogenate of the H. polygyrus complete antigen with molecular range from 11 to 130 kDa and differences in activity between fractions were observed in cell culture. In naïve mice, the percentage of apoptotic cells decreased after stimulation of MLN cells with AgS (from 51% to 34.9%) and with antigenic fractions (Figure 4a). Infection Napabucasin cost with H. polygyrus also significantly reduced the percentage of apoptotic cells. Spontaneous apoptosis in RPMI medium decreased from 51% Rucaparib supplier in uninfected mice to 22,8% after infection and only 6.3% of CD4+ cells were in apoptosis after stimulation with F9. The percentage of apoptotic cells was reduced in all examined populations

of T cells; CD4+CD25−, CD4+CD25hi, CD3+CD8+ in MLN (Figure 4b). Cells isolated on day 12 post infection responded distinctly to complete antigen (AgS) and to each antigen fraction. Treatment of cells with fraction F9, F13 and F17 deeply reduced apoptosis. In contrast, when fractions F6 and F19 were added, the percentage of apoptotic cells increased (data not shown). The lowest level of apoptosis was observed in CD3+CD4+ population. Only 5% of cells underwent apoptosis after treatment with fraction F9. Apoptosis of CD4+CD25hi and CD3+CD8+ cells was higher, 30% and 18% respectively, but was still lower in infected than in control mice (Figure 4b). Fraction F9 contrary to F17, was the most potent to reduce the percentage of apoptotic cells of infected mice. Overall, H. polygyrus somatic antigen and its fractions inhibited apoptosis (-)-p-Bromotetramisole Oxalate both in naïve and infected mice. To examine apoptosis signalling pathways, apoptosis of MLN cells was induced by dexamethasone (DEX), a synthetic corticosteroid and by rTNF-α,

and the percentage of apoptotic cells was evaluated both in uninfected and infected mice. All examined cell populations were sensitive to DEX which induced apoptosis (Figure 5). In naïve mice, 60% of CD4+ cells were apoptotic and only AgS inhibited cell death; fractions F9 and F17 even increased the percentage of apoptotic cells. Response of CD4+CD25hi cells was also significant and after treatment with DEX more than 80% of cells underwent apoptosis. After infection with H. polygyrus apoptosis of these cells was reduced by 40% and even by 60% after restimulation with the nematode antigens. CD3+CD8+ cells were less sensitive to DEX and approximately 60% of cells were apoptotic. Apoptosis of these cells was inhibited both in control and infected mice after exposition to H. polygyrus antigens.

8 years at age 60) and increasing. Further analysis is required to better define the relationship between improving survival in the dialysis and general populations. 237 THE PREVALENCE AND IMPACT OF PRURITIS IN A DIALYSIS POPULATION J HOLT1,3, S HERATH1, A LEE1,2, K MURALI1,3, M LONERGAN1,2,3, K LAMBERT1 1Wollongong Hospital, NSW; 2Shoalhaven District Memorial Hospital, Nowra, NSW; 3Shellharbour Hospital, NSW, Australia Aim: To

determine the prevalence and impact of pruritis in our dialysis population. Vincristine mouse Background: Itching is very common in patients who are on dialysis. Literature regarding the impact of pruritis on quality of life and intensity of itch is limited. Methods: The project was designed as a questionnaire.

Local Ethics approval was obtained. All patients on dialysis for ≥ 3 months area wide were eligible to participate. Participants were approached by an investigator and asked a series of questions. Routine blood results and lists of medications were also recorded. Participants were asked to rate their itch in 3 different ways: Visual Analogue Scale Lund Browder chart to estimate total body surface area involved Impact of itch on quality of life Results: 127 patients were recruited over a 3 month period.114 patients were on haemodialysis and 13 patients on peritoneal dialysis. The mean dialysis vintage was 66.9 months and the mean Saracatinib cell line duration of HD per week was 14.6 hours. 83 patients reported suffering with itch (63%) and, of these, only 35 (42%) had informed their renal physician. The mean Visual Analogue reading was 31.7 and this method of rating itch did not correlate with any of the usual biochemical parameters. The mean body surface area involved was 18% and did not correlate with the analogue reading. The presence of itch significantly impacted on the ability to fall asleep, Chloroambucil a person’s appetite and their mood, with 69% reporting feeling

unhappy either all or most of the time. Conclusions: Itch is common in patients undergoing dialysis and has a significant impact on quality of life. The majority of patients do not report their symptoms. 238 NEUTROPHIL-LYMPHOCYTE RATIO AS A MARKER OF INFLAMMATION AND PREDICTOR OF MORTALITY IN PATIENTS WITH END-STAGE KIDNEY DISEASE BL NEUEN1, N LEATHER2, A GREENWOOD2, R GUNNARSSON2, JP KILLEN1, RA BAER1, A NIGAM1, I ISMAIL1, L BERLUND1, ML MANTHA1 1Department of Renal Medicine, Cairns Hospital, Cairns, QLD; 2School of Medicine and Dentistry, James Cook University, Cairns, QLD, Australia Aim: To examine the value of neutrophil-lymphocyte ratio (NLR) as a marker of inflammation and predictor of all-cause mortality in patients with end-stage kidney disease (ESKD). Background: NLR is a marker of systemic inflammation that has been shown to predict mortality in patients with coronary and peripheral vascular disease. In contrast to albumin, NLR is unlikely to be affected by nutritional status. Its prognostic value in ESKD patients is unclear.

36 A third study provides level IV evidence that weight loss appears to be associated with a fall in total cholesterol in kidney transplant recipients.37 The recommendation that a diet rich in wholegrain, low glycaemic index and high fibre carbohydrates as well as rich sources of vitamin E and monounsaturated fat should be followed by adult kidney transplant recipients with elevated serum total cholesterol, LDL-cholesterol and triglycerides, is based on evidence from the following three studies: Stachowska et al.34

investigated the effect learn more of a modified Mediterranean diet on serum lipid levels in a single-centre, randomized controlled study. Adult kidney transplant recipients with stable graft function were randomized to receive one of two diets for a 6-month period: Treatment: Modified Mediterranean diet (n = 21; 15 males, six females), containing carbohydrates with a low glycaemic index (amylose-poor, cellulose-rich), 30 mL cold-pressed olive oil with only rapeseed oil used www.selleckchem.com/HDAC.html in cooking, foods rich in alpha-tocopherol (including nuts, grains and linseeds), fresh vegetables with each meal and

daily animal protein of 35–50 g for males and 23–46 g for females. Energy intake was attributed as follows: 47% carbohydrates, 38% fat, 15% protein. Immunosuppressive and antihypertensive regimens were not changed and no antilipemic medications were administered before or during the study during period. Dietary compliance of subjects in both groups was assessed every 4 weeks by means of 24 h food diaries and by monitoring oleic acid content of plasma triglycerides. In the treatment group, total cholesterol dropped from 230 to 210 mg/dL, or 5.9–5.4 mmol/L (P < 0.02) and triglycerides dropped from 194 to 152 mg/dL, or 2.5–1.7 mmol/L (P < 0.0007). Neither total cholesterol nor triglycerides dropped in the control group. There was no significant difference between the groups with respect to weight, body mass index and body fat levels at the

start or the end of the study period. The key limitations of this study are: the small sample size; and The study provides level III-3 evidence that a modified Mediterranean diet can be effective in lowering total cholesterol and triglycerides. The results of this study concur with the findings of studies in non-transplant populations.34 Shen et al.35 conducted a pseudo-randomized controlled study examining the effect of diet on serum lipids. They designed a diet containing less than 500 mg cholesterol, less than 35% calories from fat, less than 50% calories from carbohydrate, polyunsaturated to saturated fat ratio greater than 1, limited alcohol intake. A sodium restriction was made if the transplant recipient had hypertension.

The activating receptor NKp46 was predominantly negative on such cells, possibly as a result of encountering influenza HA. Depletion of NK cells in vivo with anti-asialo GM1 or anti-NK1.1 reduced mortality from influenza infection and surviving mice recovered their body weight. Pathology induced by NK cells was only observed with high, NVP-AUY922 not medium or low-dose influenza infection, indicating that the severity of infection influences NK-cell-mediated pathology. Furthermore, adoptive transfer of NK cells from influenza-infected lung, but not uninfected lung, resulted in more rapid weight loss and increased mortality of influenza-infected

mice. Our results indicate that during severe influenza infection of the lung, NK cells have a deleterious impact on the host, promoting mortality. Natural killer (NK) cells are large granular lymphocytes that mediate innate protection from viruses and tumor

cells [1-3]. NK cells directly lyse virally infected cells or tumor cells and produce cytokines and chemokines to attract inflammatory cells to sites of inflammation [3, 4]. Activating and inhibitory receptors expressed by NK cells regulate their functional activity. Activating NK-cell receptors include, but are not limited to, NKG2D, NKp46 (also known as NCR1), FcRγIII, Selleck Alpelisib activating Ly49 (in rodents), or activating KIR (in humans) [5, 6]. By contrast, inhibitory Ly49 or KIR and the NKG2A/CD94 heterodimer that recognize MHC class I (MHC-I) ligands or non-MHC specific receptors, such as NKR-P1b and 2B4, maintain NK-cell tolerance [5-7]. Contributions of NK cells toward resistance to viruses can be essential for host health and survival. For example, there is a correlation between humans with NK-cell deficiencies and recurrent and severe infections with varicella zoster and HSVs, respectively [8-10]. Furthermore, the expression of specific activating Ly49 by NK cells can be essential for survival of certain mouse Fossariinae strains from infection by mouse CMV [11, 12]. However, a number of reports demonstrate that NK cells can play an inhibitory role in adaptive

immunity [13-16]. In some instances, particularly during lymphocytic choriomeningitis virus (LCMV) infection, this can lead to virus persistence, as well as T-cell-mediated immunopathology [13, 14]. Thus, activities of NK cells can lead to both beneficial and detrimental outcomes from their direct and indirect influences on viral persistence and host immunopathology. Influenza viruses are one of the most common causes of human respiratory infection and are a major world health concern. Infection with seasonal or pandemic influenza virus strains lead to significant mortality [17, 18]. The most recent pandemic is from swine flu (H1N1) in 2009, a new influenza virus [19, 20]. In 2010, there were over 18 000 deaths worldwide due to this H1N1 strain [21]. Lungs require rapid and effective innate responses to prevent airborne virus infections.

To recognize their targets, NK cells use a complex array of activating receptors and/or coreceptors. These mainly include the natural cytotoxicity receptors

(NCRs, i.e. NKp46, NKp30, and NKp44), NKG2D, and DNAX accessory molecule-1 (DNAM-1). After the interaction of these receptors with their ligands (abundantly expressed by a wide variety of tumor- or virus-infected cells), NK cells exocytose click here cytotoxic granules containing perforin and granzymes, with consequent killing of the target [6-9]. Another high-powered mechanism by which NK cells can eliminate pathologic cells is the antibody (Ab) dependent cell-mediated cytotoxicity (ADCC). Targets opsonized with IgG Abs can engage CD16 (FcγRIII) on NK cells and induce cytotoxic granule release [2, 10]. Although the ability of NK cells to eliminate pathologic cells has been demonstrated in vitro and in certain animal models [5, 11-14], there are still many obstacles for the effective use of these cells in immunotherapy. Both tumors and viruses have developed different escape mechanisms

to avoid NK-cell immunosurveillance. For example, certain viruses can shape the expression profile of various NK-receptor ligands in infected cells [15]. Similarly, tumor cells may shed from the surface certain NKG2D-ligands thus avoiding NK-cell-mediated attack [16]. In addition, several lines of evidence indicate that the tumor microenvironment may impact the real ability of NK cells to clear pathologic cells [17-22]. Indeed, while cytokines such as IL-2, IL-15, IL-12, and IL-21 can enhance NK-cell function, other factors induced Fulvestrant chemical structure at the tumor site,

such as IDO, PGE2, and TGF-β, or even the direct interaction with tumor cells or tumor-associated stromal cells, may impair the cytotoxic activity of NK cells [23-26]. A common feature of the tumor microenvironment and one of the major drivers behind tumor progression, resistance to therapy, immunosuppression, and bad prognosis is hypoxia, a condition of reduced partial O2 tension (pO2), which arises as a result of disorganized or dysfunctional Anacetrapib vessel network [27, 28]. Response to hypoxia is under the molecular control of a family of hypoxia-inducible transcription factors (HIFs), composed by the constitutive HIF-1β subunit and an O2-sensitive α subunit (HIF-1α or -2α), which is stabilized by the decrease of O2 levels. HIF transactivates the hypoxia responsive element present in the promoter of many hypoxia-inducible genes, including those involved in tumor cell proliferation, angiogenesis, invasion, metastatic spread, and drug resistance [29-31]. Low oxygen tension also occurs at sites of infection. Recent studies documented the contribution of hypoxia to the outcome of viral infection by affecting the activity of viral proteins, virus replication, and evasion of host immune responses through HIF-1α induction [32-35].

65 Not surprisingly, NGAL measurements as an outcome variable are currently included in several ongoing clinical trials formally listed in ClinicalTrails.gov. The approach of using NGAL as a trigger to initiate and monitor novel therapies, and as a safety biomarker when using potentially nephrotoxic agents, is expected to increase. It is also hoped that the use of predictive and sensitive biomarkers such as NGAL as endpoints in clinical

trials will result in a reduction in required sample sizes, and hence the cost incurred. A number of studies have demonstrated the utility of early NGAL measurements for predicting the severity and clinical outcomes of AKI. In children undergoing cardiac surgery, early post-operative plasma NGAL levels strongly correlated with duration and severity of AKI, length Tipifarnib manufacturer of hospital stay

and mortality.66 In a similar cohort, early urine NGAL levels highly correlated with duration and severity of AKI, length of hospital stay, dialysis requirement and death.67 In a multicentre study of children with diarrhoea-associated haemolytic uraemic syndrome, urine NGAL obtained early during the hospitalization predicted the severity of AKI and dialysis requirement with high sensitivity.68 Early urine NGAL levels were also predictive of duration of AKI (AUC 0.79) VEGFR inhibitor in a heterogeneous cohort of critically ill paediatric subjects.51 In adults undergoing cardiopulmonary bypass, those who subsequently required renal replacement therapy (RRT) were found to have the highest

urine NGAL values soon after Olopatadine surgery.30–37 Similar results were documented in the adult critical care setting.53–59 Collectively, the published studies revealed an excellent overall AUC-ROC of 0.78 for prediction of subsequent dialysis requirement, when NGAL was measured within 6 h of clinical contact.41 Furthermore, a number of studies conducted in the cardiac surgery and critical care populations have identified early NGAL measurements as a very good mortality marker,30–32,54,55,59 with an overall AUC-ROC of 0.71 in these heterogeneous populations.41 Furthermore, there is now evidence for the utility of subsequent NGAL measurements in critically ill adults with established AKI. Serum NGAL measured at the inception of RRT was an independent predictor of 28-day mortality, with an AUC of 0.74.69 With respect to the sample source, the majority of AKI biomarkers described thus far have been measured in the urine. Urinary diagnostics have several advantages, including the non-invasive nature of sample collection, the reduced number of interfering proteins, and the potential for the development of patient self-testing kits.

A prime example of this was the discovery of the epistatic interaction between CARD15 and the T300A allele of ATG16L1 in CD 50, 51 and the identification of risk loci in the autophagy gene IRGM52, 53. This has shed light on Selleckchem BMN 673 autophagy as a potential mechanism in CD pathogenesis. Indeed, recent data have started to uncover the role of autophagy in NLR innate immune response to pathogens. Travassos et al. have demonstrated that NOD1 and

NOD2 linked bacterial sensing to the initiation of autophagy through ATG16L1, independently of RIP2 and NF-κB signaling 54. Although WT NOD2 recruited ATG16L1 to bacterial entry sites and induced autophagy, L1007insC mutant NOD2 failed to do so. Interestingly, cells from donors homozygous for the ATG16L1 T300A

risk allele had impaired induction of autophagy and bacterial clearance when stimulated with NOD2 agonists despite colocalization of ATG16L1 with NOD2 54. This suggests that the ATG16L1 polymorphism might affects the recruitment and activation of other autophagy-related Trametinib in vivo proteins or modulate the stability of the ATG16L1 protein 55, leading to unchecked TRIF-dependent activation of caspase-1 and increased production of IL-1β and IL-18 56. Clearly, additional functional studies are now required to place all of the new risk loci identified by GWAS into a meaningful biological context that will enable an understanding of their roles (if any) in normal NLR homeostasis and pathogenesis of autoinflammation. It is also hoped that GWAS design that integrate new technologies including SNP arrays with better SNP coverage (currently limited to ∼70% of the common sequence variation in European populations), high-resolution comparative genomics, and next-generation

sequencing will continue to enable the dissection of this complex disease and help solve its “missing heritability. The genetic characterization of auto-inflammatory disorders such as the inflammasomopathies has not merely enhanced our understanding of NLR biology but has also highlighted AMP deaminase the ability of the inflammasome to cause a large number of inflammatory diseases without major provocation of the adaptive immune system. The story is far more complex in the case of CD. Progress in the search for new inflammatory disease loci may reveal proteins involved in the homeostatic pathways guarded by the NLR. This has the potential to provide answers of how proteins like NLRP3 sense a plethora of disparate activators. For example, recent studies of AIM2, a susceptibility factor for systemic lupus erythematosus, have discovered the first direct interaction between an inflammasome sensor (AIM2) and its ligand (cytoplasmic DNA) 57–59.

Moreover, we have recently shown that histamine stimulates both the uptake and the cross-presentation of antigens by DCs, supporting the theory that histamine promotes activation of CD8+ T

cells during the development of allergic pathologies. Here, we investigated whether the course of an allergic response, in a well-defined model of ovalbumin (OVA)-induced allergic airway inflammation, could be modulated by intratracheal Ipatasertib mouse injection of OVA-pulsed DCs previously treated with histamine (DCHISs). Compared with control DCs, DCHISs induced: (i) greater recruitment of CD8+ T cells in the lung, (ii) greater stimulation of the production of interleukin (IL)-5 by lung CD8+ T cells, and (iii) increased recruitment of CD11c/CD8 double-positive DCs in the lungs of allergic mice. Moreover, mice treated with DCHISs showed increased levels of serum-specific immunoglobulin E (IgE) antibodies directed to OVA, and a higher proportion of eosinophils in bronchoalveolar lavage (BAL) compared with mice treated with OVA-pulsed control DCs. Our results support the notion that histamine, by acting on DCs, increases the severity of allergic processes.

Dendritic cells (DCs) have the unique ability to activate resting T lymphocytes and play a critical role not only in the priming EGFR activation of adaptive immune responses, but also in the induction of self-tolerance.1,2 Upon stimulation by inflammatory stimuli or pathogens in the periphery, DCs undergo a number of changes, leading to their maturation.3 Mature DCs activate naïve T cells and direct the differentiation of CD4+ T cells into cells with distinct profiles.1–4 Histamine (HIS) plays an important role in the development of lung inflammation during the course of allergic processes by inducing airway constriction, mucus secretion PIK3C2G and recruitment of immune cells.5,6 Histamine

is involved in the regulation of DC function. It stimulates the chemotaxis of immature DCs,7,8 increases the ability of DCs to induce the differentiation of CD4+ T cells into cells with a T helper type 2 (Th2) profile,9 and induces the cross-presentation of antigens by DCs through major histocompatibility complex (MHC) class I,10 supporting the theory that histamine plays a role in the activation of CD8+ T cells in response to allergens. Adoptive transfer of allergen-pulsed DCs is a useful tool with which to examine the role of DCs in the course of allergic lung inflammation.11,12 It has been shown that injection of antigen-pulsed DCs into the airways leads to sensitization to inhaled antigen and to the development of antigen-induced airway eosinophilia.12–14 Moreover, modulation of the functional profile of DCs has been shown to be able to regulate the course of allergic inflammation.