[5] Both genera are ubiquitous in the environment with high prevalence

in tropical and sub-tropical regions, particularly in equatorial Africa, Central America and India.[6] Entomophthoromycosis has a predilection for areas with adipose tissue, possibly because these organisms thrive on fatty substances.[7]The disease presents in two clinically distinct forms; basidiobolomycosis (subcutaneous zygomycosis) and conidiobolomycosis (rhinofacial zygomycosis). Neither of these two forms occurs preferentially in patients with underlying disease or defective immunity.[8] Basidiobolus was first described by Eidam in 1886. It is a filamentous fungus isolated from amphibians, reptiles, horses, dogs and bats, as well as wood lice, plant debris and soil.[9] Basidiobolus is classified into B. ranarum, B. meristosporus and B. haptosporus. However, the taxonomic studies based on antigen analysis and restriction PARP inhibitor enzyme analysis revealed that all human-pathogenic isolates belong to B. ranarum.[10, 11] The first case click here of subcutaneous mycosis caused by B. ranarum in humans was reported from Indonesia

in 1956.[12] After that, many cases of subcutaneous basidiobolomycosis have been reported from different parts of Africa (especially Uganda and Nigeria), India and South-East Asia.[13, 14] The infection is thought to occur following traumatic implantation of the fungus into the subcutaneous tissues of the thighs, buttocks or trunk. This form of zygomycosis occurs predominantly in children (80% below the age of 20 years) with a male/female ratio of 3 : 1.[13, 15] The disease manifests as disc-shaped, rubbery, mobile masses that may be quite large and are usually located in the shoulder, hips or thighs.[13, 16] The lesions contain inflammatory Fossariinae cellular material with many eosinophils, accounting for the skin erythema and warmth.[17] The condition is slowly progressive but seldom life threatening.[18] Painless firm erythematous plaques of the subcutaneous tissue

are also characteristic of the disease.[13] Significant non-pitting oedema of the involved area may occur. Additionally, skin ulceration and lymph node enlargement may be observed.[19, 20] The main differential diagnoses of these lesions are tuberculosis, localised elephantiasis, onchocerciasis, scleroderma, Burkitt’s lymphoma and Wegener granulomatosis.[21] Systemic dissemination is extremely uncommon[22]; however, widespread fatal dissemination had been reported in a previously healthy woman, with involvement of brain, lung, spleen, stomach, kidney and pancreas.[23] Basidiobolomycosis rarely involves extracutaneous systems. Gastrointestinal basidiobolomycosis (GIB),[24] retroperitoneal [25, 26] and pulmonary [23] basidiobolomycosis have been reported in the medical literature. The first case of GIB was reported in 1964 in a 6-year-old Nigerian boy.

All other DC populations had a slightly better ability to stimulate T cells. The maturation status of DC has an important role in initiating and directing antitumor immune responses [26]. A proper mature DC population is essential, because the quality of the DC vaccine-induced immune response never can be better than the quality of the DC population used. DC used in most clinical trials today are stimulated with the Jonuleit cytokine cocktail [13] referred to as the ‘gold standard’.

The discussion concerning this cytokine cocktail is related to the use of PGE2. This inflammatory mediator has been shown to augment survival [27] and migration [28] of DC, in addition to be responsible for surface expression of the costimulatory molecules CD252 (OX40L) and CD70 needed for the stimulation of T cell proliferation [29]. However, PGE2 has also been demonstrated to be responsible for Wnt inhibitor the lack of secreted IL-12p70 [17, 18], which INK 128 datasheet is crucial for the activation of strong immune responses through the induction of Th1-type responses. The intentions behind this study were to analyse the effect of bromelain on DC maturation and to investigate whether bromelain could replace PGE2 in the cytokine cocktail to overcome

the negative effects of PGE2. Previous experiments performed with bromelain on glioma cells had shown that bromelain affects and alters glioma cells without causing any cellular toxicity at 50 μg/ml [23]. This was only partly confirmed during our experiments, as DC treated with 100 and 50 μg/ml of bromelain showed lower viability compared with cells treated with lower concentrations of bromelain. Stimulation with 25 μg/ml bromelain resulted in phenotypic mature DC that secreted more IL-12p70 than DC matured with the cytokine cocktail. When bromelain was combined with the cytokine cocktail, we discovered the existence of a synergistic effect, influencing the expression of some of the analysed surface markers. Clearly, higher levels of CCR7 and CD83 were detected when using bromelain in combination with the original cytokine cocktail or bromelain

in combination with the cocktail with reduced amount of PGE2 as maturation stimulus. This synergistic effect was lost when bromelain was used in combination with the cytokine Obatoclax Mesylate (GX15-070) cocktail without any PGE2. The migratory capacity of DC has been shown to be dependent on their surface expression of CCR7 [30], although we could recently show that CCR7 is not directly correlated with its ligand CCL19-driven chemotaxis [24]. PGE2 was shown to be responsible for the upregulation of CCR7 on the surface of DC [16]. In addition to the effect of CCR7 expression on DC, PGE2 was found to be important for induction of metalloproteinase-9, which is also important for the migration of DC [31]. This is consistent with our data, showing that surface expression of CCR7 is strikingly reduced when PGE2 is completely removed from the cytokine cocktail.

[53] conducted case–control study including SARS-infected patients, health care workers and controls. They found no differences in TNF-α genotype distribution at the rs1799964, rs1800630, rs1800629 and rs361525 among the three populations. The CT and CC genotypes of rs1799964 were associated with a risk effect on femoral head necrosis. The rs1800630 AC genotype was another risk effect associated with femoral head necrosis in cured SARS-infected patients compared to CC genotype. Severe dengue virus infection.  Cascade of cytokine produced included TNF and LTA in severe

dengue virus (DENV) infections. The TNF rs361525 BMN 673 mouse A polymorphism marking the TNF-4, LTA-3 haplotype, was significantly increased in patients with secondary dengue haemorrhagic fever (DHF) compared to those with secondary dengue fever (DF) in Thais [54]. Two extended MHC haplotypes containing TNF-4 and LTA-3, together with HLA-B48, B57 and DPB1*0501, have been reported only in patients with secondary DHF. These observations indicate that polymorphism in functionally distinct MHC-encoded proteins contributes to the risk of developing severe secondary DENV infection. Guivier et al. [55] found that two SNPs within the TNF-alpha promoter (−302GG/GG and −296A/A) were associated with

higher TNF-α gene expression and were more frequent in non-endemic areas among European populations of bank voles. Plasmodium falciparum malaria. Malaria is the most common parasitic disease of the tropics caused by the sporozoa of the genus Plasmodium, is endemic in more than 90 countries, and together with HIV and tuberculosis constitutes one of the major causes of death by infectious diseases worldwide. Erismodegib Monoiodotyrosine During P. falciparum malarial infection, TNF has been described as both protective and pathogenic, and at low levels, TNF kills the parasite by macrophage activation and subsequent release of cytokines, whereas high TNF level has been associated with severe manifestations like acute respiratory distress and cerebral malaria. It has been reported that SNPs (rs1799964, rs1799724, rs1800750, rs1800629 and rs361525) in the proximal enhancer of the TNF gene have different associations with

malaria in different populations [49, 56–58]. Sinha et al. [59], genotyped these SNPs in patients with P. falciparum malarial infection and controls in Indian population. They found association of the rs1799964 and rs1800630 with increased risk of severe malaria. TNF enhancer haplotype CACGG (rs1799964, rs1800630, rs1799724, rs1800629 and rs361525) correlated with enhanced plasma TNF levels in both patients with falciparum malarial infection and controls and were associated with increased susceptibility to severe malaria. No association between rs1800629 polymorphism and susceptibility to cerebral malaria among central Sudanese children was reported [60]. Mucocutaneous leishmaniasis.  Leishmania braziliensis infection is responsible for MCL. It is a severe form of American cutaneous leishmaniasis (ACL).

maxima APGA could induce cross-protection

to heterologous species, E. tenella and E. acervulina, as well as E. maxima infections (68,69). At this point, it was believed that this cross-reactivity was most probably due to conserved epitopes of the major gametocyte antigens in the different species and, thus, led to the hypothesis that a vaccine of E. maxima gametocyte antigens could possibly be used to control coccidiosis caused by at least the three predominant Eimeria species. In floor pen maternal immunization trials, the resistance of chicks from APGA-immunized breeder hens was compared to that of hatchlings from control parent flocks by introducing oocysts to the pens via infection of ‘seeder’ birds infected with 50 oocysts of E. maxima, R428 purchase E. tenella and E. acervulina. Analogous to the laboratory trials, a reduction of 60–80% in oocyst shedding into the litter was observed; comparable to the reduction observed using coccidiostats (59). These buy Selumetinib trials were repeated three times under the same conditions, showing that there was an average reduction of 60–70% oocyst output in vaccinated groups up to 4–6 weeks in age (59,70). These results were encouraging, as they supported the idea that the highly conserved E. maxima antigens could provide good levels of protective immunity against at least three major species

that cause coccidiosis in broilers. Despite this, questions still remained about whether this vaccine could provide maternal protection against all Eimeria species (and strains) encountered in the field and if maternal immunity was applicable in controlling coccidiosis

within industry management schemes and climatic conditions. To further assess the efficacy of maternal immunization with APGA, testing was undertaken in a multi-centred, multinational field trial involving five countries from four different continents: Israel, Brazil, Argentina, South Africa and Thailand (71,72). The safety and immunogenicity of the vaccine in breeding hens were assessed on a large scale, with birds vaccinated twice prior to the start of their laying period (15 and 20 weeks respectively). Immunizations were found to have no deleterious effect on the hens (72): no adverse reactions; no damage at the site of injection; and no affect on hen mortality or on the number P-type ATPase of eggs produced (e.g., in the Argentine trials, 119 eggs were produced per immunized hen vs. 116 per control hen). In all four countries, IgG antibody titres remained at a presumptive protective level throughout the life of the laying hens. The maintenance of highly specific IgG antibody levels in vaccinated flocks is thought to be due to the boosting effect that is naturally acquired from exposure to infection with oocysts in the environment (72). It is even conceivable that maternal antibodies may increase due to this natural exposure. However, in the absence of immunization, these titres are variable and, therefore, do not necessarily provide protective levels of maternal immunity (72).

This result contrasts with the effects of simvastatin on SOCS3 induction that were maximal after 24 hr of stimulation. When we examined the effects of simvastatin on the early events in the TGF-β signal transduction cascade, we did not observe any augmentation of Smad3 phosphorylation. In contrast, the major effects of simvastatin were associated with a decreased induction of Smad6/7, inhibitory Smads that inhibit TGF-β signalling by blocking the phosphorylation of Smad2/3.

We favour the view that simvastatin can directly block the induction of Smad6/7 expression, as the drug also inhibited the induction of Smad6/7 at 72 hr in the presence of a TCR signal alone in the absence of TGF-β. Alternatively, it is possible that the effects of simvastatin on Smad6/7 expression are mediated indirectly via a direct effect on Foxp3 expression as Fantini et al.22 have selleckchem demonstrated that transfection of Foxp3 is capable of blocking TGF-β-induced Smad7 expression by acting directly on the Smad7 promoter. This mechanism is consistent with our findings that Smad6/7 cannot be induced in Foxp3+ nTregs following TGF-β signalling. Although it is difficult to extrapolate from our in vitro model systems to the in vivo situation, our results that simvastatin can markedly

enhance the induction of Foxp3 expression BMN673 in the presence of Selleck Fludarabine low concentrations of TGF-β strongly suggest that some of the beneficial effects of simvastatin include the generation of Tregs in the inflammatory milieu of the atherosclerotic

plaque. Further analysis of the mechanism of action of simvastatin will require identification of the targets of geranylgeranylation at different time-points after T-cell activation. Ras, Rho, CDC42 and many different GTPases are important for early signal transduction after engagement of the TCR and may play a role in induction of SOCS3. However, our findings suggest that the effects of simvastatin are on proteins synthesized 24 hr after TCR stimulation. At the very least, our study strongly implies that an analysis of TCR-specific protein prenylation is a potential pathway for pharmacological manipulation of Tregs in vivo. This study was supported by the Intramural Research Program of the National Institute of Allergy and Infectious Diseases, National Institutes of Health (Bethesda, MD). The authors have no conflict of interest. Figure S1. Simvastatin does not induce cell death or alter the cell cycle of Foxp3− cells. “
“The composition of the peripheral blood lymphocyte compartment underlies developmental changes during ontogeny. Recently, several new B cell populations have been characterized which were suggested to develop in an age-dependent manner. However, age-dependent reference values for distinct B cell populations have rarely been reported.

0 mg/dL) levels were high, although other IgG subtypes were normal. Serum immunofixation did not demonstrate M protein, and the level of serum soluble IL-2 receptor was normal. The serum levels of κ (20.6 mg/dL) and λ (18.5 mg/dL) free light chains and the κ/ λ ratio (1.11) were also normal. The patient also did not have any donor specific antigens. A contrast-enhanced CT scan revealed a non-enhanced mass at the renal hilum

and some contrast defect areas in the renal cortex and diffuse marked enlargement of the graft, although no lymph node swelling was observed (Fig. 2A). An MRI also showed a hilum mass lesion with high intensity on T2-weighted images check details and low intensity on diffusion-weighted images. A PET-CT scan only detected a light integrated

mass of the hilum. Based on these findings, the patient was suspected of having IgG4-RKD. As the renal function of the patient was stable at that time, a no-treatment follow-up strategy was considered appropriate. However, her renal function deteriorated gradually and the serum Palbociclib chemical structure IgG4 level remained high (>400 mg/dL). In November 2012, the patient’s serum creatinine level had increased to 1.56 mg/dL. A biopsy was therefore carried out that showed almost the same findings as the biopsy 2 years after transplantation, although some severe fibrotic lesions and infiltration of IgG4-positive plasma cells were observed directly under the renal capsule. Because of the deterioration in renal function, the methylprednisolone dose was increased to 16 mg/day. Three months after this increase in steroid dose, the hilum mass disappeared on a CT scan (Fig. 2B), but cytomegalovirus antigenmia, JC virus viruria and viraemia screening became positive. An over-immunosuppression state was therefore suspected, and the methylprednisolone dose was decreased to 8 mg/day and mycophenolate mofetil changed to mizoribine. 4-Aminobutyrate aminotransferase Five months after the initial increase in steroid

dose, a follow-up biopsy in May 2013 showed that plasma cell infiltration in the renal interstitium had decreased markedly, although focal and segmental severe interstitial fibrosis and tubular atrophy with IgG4-positive plasma cells were observed (Fig. 3). Serum IgG4 levels decreased immediately after the increase in steroid dose and remained at <100 mg/dL thereafter. The patient's serum creatinine level also remained stable at around 1.6 mg/dL. The clinical course of the patient is shown in Figure 4. IgG4-RKD usually manifests as plasma cell-rich tubulointerstitial nephritis (TIN), although its clinicopathological features are not well described. Raissan et al. showed that most patients with overt IgG4-RKD had acute or progressive chronic renal failure, involvement of other organ systems, radiographic abnormalities such as small peripheral low-attenuation cortical nodules or diffuse marked enlargement of the kidneys, and elevated IgG4 serum levels (>135 mg/dL).

Overall, RAS or CPS immunizations resulted in sporozoite-specific IFNγ responses in the liver (P = 0.03) and spleen (P = 0.008). Although not reaching statistical significance, there was a tendency of higher sporozoite-specific IFNγ response by

T cells with memory phenotype (CD44hi) in liver and spleen (Figure 2b) cells from IV immunized compared to ID immunized C57BL/6J mice. Within the T-cell population, similar observations were made for CD8+CD44hi T cells. Furthermore, the levels of CD8+ Tem cells in both IV and ID groups correlated with the IFNγ response in liver (R = 0.63, P = 0.003) and spleen (R = 0.54, P = 0.01). Three weeks after challenge, the observed high levels of liver CD8+ Tem cells (Figure 2c) and increased IFNγ responses (Figure 2d) were sustained in Selleckchem AP24534 IV immunized mice. No data were obtained from ID immunized mice as these did not

survive challenge infection (Table 1). Finally, functionality of RAS- and CPS-induced antibodies was tested in the sporozoite neutralization assay, testing their capacity to invade and subsequently develop in liver cells (24). Sporozoite invasion was strongly reduced in the presence of plasma from both RAS and CPS immunized mice (P ≤ 0.05), with stronger inhibition by IV immunized mice within the RAS group (P < 0.01) (Figure 3). As CPS ID immunized mice showed similar blocking activity compared to IV immunized mice, antibodies may contribute but are by themselves likely not selleck inhibitor sufficient

to induce complete protection. Our findings show that ID immunization Tryptophan synthase with whole live malaria parasites confers a far lower protective efficacy when compared to IV immunization. The reduced protective efficacy clearly associates with a lower number of sporozoites reaching the liver. Lower protective efficacy by ID immunization was observed in both BALB/c and C57BL6/j mice using two independent immunization protocols, that is, sporozoite liver cell invasion only with early developmental arrest (RAS) or full completion of liver maturation and early abrogation of blood-stage multiplication (CPS). Moreover, both RAS and CPS IV immunizations induce higher cellular immune responses compared to ID. Our data confirm the earlier formulated hypothesis by Epstein et al. (18): based on low hepatic immune responses in ID immunized animals and low protection level in a clinical trial, the authors suggest that the degree of parasite liver load following sporozoite administration associates with protective efficacy. However, ID immunization can induce high levels of protection provided that sufficiently high numbers of sporozoites (i.e. 9 × 104P. yoelii) are injected (17). The necessity of high numbers of sporozoites for ID induced protection supports the notion that liver parasite load might be important for protective efficacy of whole sporozoite immunization. ID injection of P.

Seven of eight patients survived Aspergillus endocarditis when heart valve surgery was performed (valve replacement, resection of vegetations) while only 1/17 survived with conservative treatment alone. Interestingly, 74% of the patients included in this analysis had a history of recent surgery, 68% of which had heart surgery performed, suggesting recent heart surgery as a risk factor for Aspergillus contamination of the endocardium during surgery. 5-Fluoracil clinical trial Aspergillus pericarditis is rare and usually develops

from adjacent infected tissue, such as an expanding pulmonic Aspergillus focus, from spreading Aspergillus myocarditis or by surgical contamination. As published in a review evaluating 29 cases, Aspergillus infection of the pericardium was always the result of contiguous dissemination of the lung or myocardium.

In that review only four of the 29 reported patients survived the infection.[66] Diagnosis selleckchem of Aspergillus pericarditis is challenging, which may be a reason for frequently delayed decision for surgery. Electrocardiogram and echocardiography are the investigations of choice. They may show signs of pericardial effusion or thickening of the pericardium. However, these investigations may also appear normal. Only in 10 of the 29 cases, the pericarditis was correctly diagnosed before death and in all of these 10 cases Aspergillus infection affecting other organs had already been diagnosed before. Rapid pericardiectomy and/or surgical drainage under systemic antifungal therapy is recommended to prevent cardiac-related death and to gain tissue for diagnostics. Pericardial tamponade, haemodynamic deterioration and cardiac arrest DCLK1 due to arrhythmia[66-68] contribute to the reported fatal outcome. In a study published in 2000 by Silva et al. [69], eight cases of culture proven Aspergillus infection of an aortic aneurysm – all without prior surgery – were

investigated. All eight patients received surgical intervention; however, only three patients survived. Interestingly the three patients, who survived received all a resection of the aneurysm with in situ graft replacement, whereas the five patients who died, only had smaller surgery like embolectomy, indicating that resection of the mycotic aneurysm is crucial for outcome. In most patients of that study, the suspected primary focus of Aspergillus infection was the lung, spreading via vascular invasion. Primary Aspergillus infection of the lung can lead to erosion of the tissue and building of aortobronchial fistula, presenting clinically with haemoptysis. In these cases, partial pneumectomy and resection of the affected vessels are necessary.[69, 70] Aspergillus aneurysms of the aorta have also been reported to be caused by prior surgical interventions, either during cardiac valve replacement or grafting of aortic dissection, resulting in major complication and life-threatening embolic events.

Sorted mDC were 70–80% pure, with 5–20% monocytes and less than 1% pDC C646 cost contamination. Probe-based quantitative PCRs were designed using the human Universal Probe Library design center (Roche Applied Science, Penzberg, Germany). Real-time quantitative PCRs (qPCRs) were performed on the CFX96™ real-time PCR detection system (Biorad, Herts, UK) using iTaq Supermix with Rox (Biorad) and the following primer (Invitrogen/Life Technologies, Paisley, UK) and probe (human Exiqon probe library; Roche, Woerden, the Netherlands) combinations: IL-12p40 5′-CCACATTCCTACTTCTCCCTGA-3′ and 5′-ACCGTGGCTGAGGTCTTGT-3′ with

TCCAGGTC fluorescent probe, TNF-α 5′-AAGCCTGTAGCCCATGTTGT-3′ and 5′-GCTGGTTATCTGTCAGCTCCA-3′, with CCAGGAGG fluorescent probe and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) 5′-CAACGAATTTGGCTACAGCA-3′ and 5′-GTGGTCCGGGGGTCTTAC-3′ with CCACCACC fluorescent probe. IL-12p40 and TNF-α mRNA expression levels were standardized to reference gene GAPDH mRNA expression levels using the Pfafll method [31]. The non-parametric Mann–Whitney U-test was used to determine the statistical selleck chemical significance of cell numbers and TLR-induced cytokine expression in rhesus macaque versus human DC subsets and monocytes. As published

previously [16, 24], pDC and mDC subsets can be distinguished in peripheral blood of rhesus macaques on the basis of CD11c versus CD123 expression in HLA-DR-positive cells, which are negative for lineage markers CD3, CD8, CD16, CD20 and CD14 (Fig. 1). However, comparison of the dot-plots

shown in Fig. 1 (right graphs) reveals a striking difference in the percentage of pDC relative to mDC in the lineage–, HLA-DR+ cells in human versus rhesus macaque blood. As shown in Fig. 2, analysis of a larger cohort showed that the absolute number of pDC was significantly lower in rhesus macaques (3020 ± 1357 cells/ml) than in humans (10 495 ± 4353 cells/ml), while there was no difference in the number of mDC (20 811 ± 14 361 versus 17 178 ± 5671 cells/ml) or monocytes (324 000 ± 161 000 versus 217 000 ± 107 000 cells/ml). In order to evaluate the function of IMP dehydrogenase peripheral blood DC subsets in rhesus macaques without interference of cell isolation procedures, a whole blood stimulation assay was used, analogous to the previously described assay for human blood DC [29]. In brief, heparin blood was diluted 1:5 in RPMI-1640 medium with 0·1% bovine serum albumin (BSA), heparin and β-mercaptoethanol. Samples were exposed for 8 h to different TLR ligands and the cells were then stained and analysed by flow cytometry for the induction of maturation markers and cytokine expression. This procedure has the advantage that it allows detection of the response of different DC subsets simultaneously in one tube. Time–course experiments showed optimal induction of cytokine expression after 5–8 h incubation with all selected TLR-7/8 (CL097), TLR-9 (CpG-C) and TLR-4 (LPS) ligands (Fig. 3).

The specificity of this observation was underlined by control experiments, in which the use of serum from mice sensitized

against a different antigen did not result in increased T-cell activation when FcR γ-chain deficient DC were used. This largely excludes the possibility that circulating inflammatory factors, such as amyloid P or C reactive protein 26, in sensitized this website mice could account for the results. Furthermore, it confirms that FcγRI, FcγRIII or FcγRIV are required for augmented antigen presentation and also that lung DC lacking these receptors are devoid of constitutively defective processing or presentation via MHC class II. Considering that OVA-specific IgG1 is generated during sensitization 13 and given the fact that IgG1 binding by activating FcγR is exclusively dependent on FcγRIII 27–29, with no contribution of FcγRI and FcγRIV 11, 30, we speculate that FcγRIII is the major mediator of these effects. Further

studies using targeted knock down of FcγR on Selleck ABT 888 DC after sensitization or Th2 cell transfer might help to further delineate the function and contribution of these effects to pulmonary hypersensitivity. We assumed that under physiological conditions the formation of immune complexes would have a preferential impact on activation and antigen presentation of lung DC 17, 18 and thus examined DC outside secondary lymphoid organs. Further studies are required in order to identify specific lung DC subsets that might be involved in this process

28 and to investigate whether other Fc-receptor expressing cells contribute to this effect. It seems likely that migratory and resident LN DC populations could be regulated through IgG in a similar way. This would have important Galeterone implications, not only for the priming of antigen-specific allergic T-cell responses and the re-challenge of existing T-cell populations, but presumably also on the collateral priming to inhaled antigens 4. In this respect, the DC activation and cytokine production following engagement of activatory FcγR could be of further relevance. It is important to note, however, that allergen-specific IgG can also alleviate the strength of a pulmonary hypersensitivity reaction, presumable by modulationg macrophage function through FcγR 31. In summary, we conclude that not only IgE but also IgG and FcγR play an important role during the manifestation of allergen-induced airway hyperresponsiveness and inflammation. In addition to their function during sensitization against allergens, FcγR-mediated enhanced antigen presentation and T-cell stimulation by lung DC appears to have a significant impact on inflammatory responses during the airway challenge phase. These data support therapeutic strategies that target FcγR for the treatment of asthma.