It is well

known that the inflammatory response inhibits fibrinolysis, which contributes to the prothrombotic state seen in conditions such as sepsis [16], inflammatory bowel diseases [17] and rheumatoid arthritis [18]. However, to the best of our knowledge, no data are available concerning systemic fibrinolysis in BP patients, although it has been shown to be involved at local level LDK378 mw in lesional skin in humans and experimental BP models [19-23]. With this background, we evaluated systemic fibrinolysis by measuring the plasma parameters of 20 patients with BP in an active phase and in clinical remission after systemic corticosteroid treatment, and correlated the results with coagulation

markers and the parameters of disease activity. We conducted an observational study enrolling 20 consecutive patients with previously untreated active BP (10 males and 10 females; mean age 76 years, range 53–99) who were admitted to our Dermatology Department from January 2010 to June 2011. The diagnosis of BP was established on the basis of clinical and immunopathological criteria. All the patients had a clinical picture of generalized BP without any mucous membrane involvement GW 572016 (mean disease duration: 1 month, range 0–2); the skin lesions (vesiculobullous and/or erythematous–oedematous lesions) covered a median 40% of total body area (range 20–60%). Direct immunofluorescence examinations of the perilesional skin revealed the linear deposition of IgG and/or C3 in the BMZ in all cases, Alanine-glyoxylate transaminase circulating anti-BP180 autoantibodies were detected by means of an ELISA. Concomitant neoplastic or inflammatory diseases were excluded on the basis of clinical and instrumental examinations. None of the patients had thyroid dysfunction or atrial fibrillation and were taking drugs affecting coagulation. Three of the 20 BP patients had type 2 diabetes and were receiving treatment with oral anti-diabetic drugs with an acceptable

disease control (haemoglobin A1c values 6·5, 6·7 and 7·0, respectively). After taking the blood samples, patients with active disease were treated with methylprednisolone at an initial dose of 0·5–0·75 mg/kg/day. When either new lesions or pruritic symptoms have not occurred for at least 2 weeks, the tapering of steroid was started until reaching the minimal dose of 0·05–0·1 mg/kg/day. All the patients were also studied during clinical remission, defined as the absence of any new BP lesions with the complete healing of the previous lesions for a minimum of 4 weeks. At the time of sampling, they were being treated with low-dose corticosteroids (methylprednisolone 4 mg daily). The control group consisted of 20 age- and sex-matched apparently healthy subjects with no history of thrombosis (10 males and 10 females; mean age 75 years, range 55–94).

The first dose is given under observation in the clinic and, if tolerated, the patient can then self-administer the treatment daily at home. Clinical follow-up to encourage compliance, monitor for adverse events and to adjust any medical treatment is still recommended. Efficacy parameters.  There are no efficacy parameters or biomarkers that reliably predict or indicate response to treatment [18]. Responses Napabucasin purchase in clinical trials have been assessed using symptom and medication scores and measuring quality of life using a validated questionnaire. Long-term efficacy has been shown with SCIT to grass pollen.

Patients who received treatment for a period of 3 years showed sustained benefit for 7–9 years following discontinuation of desensitization [13,31–34]. VIT is the only specific treatment currently available to reduce the severity and prevent the recurrence of systemic reactions (SR) in patients with a previous history of life-threatening SR or anaphylaxis to hymenoptera

insect sting [35–39]. It is highly effective, providing more than 90% protection from reactions to subsequent stings [35,40–42]. Furthermore, it induces a clinically significant improvement in health-related quality of life both in patients with a history of anaphylaxis as well as those click here with non-life-threatening SRs to hymenoptera stings [43,44]. For a successful clinical outcome in VIT a systematic approach with a good clinical history, and in some cases scrutiny of hospital records relating to previous reactions, are paramount. Knowledge of the insect involved is valuable in making the correct choice of venom. Honey bees usually leave the barbed

stinger behind, whereas wasps and hornets usually do not. Details of the circumstances surrounding the sting episode may also provide useful pointers with respect to the nature of the insect. Indications (Table 2).  Anaphylaxis to hymenoptera sting represents a clear indication for VIT [36–38]. However, in patients with non-life-threatening reactions other risk factors such as age, co-morbid conditions, occupation, hobbies, social circumstances and the patient’s own choice must be considered carefully prior to making a decision Sitaxentan about pursuing VIT. Demonstration of venom-specific IgE is mandatory prior to initiating VIT. Venom immunotherapy is not indicated in patients with local reactions, irrespective of their severity, and further investigations are not warranted [36–38]. VIT must not be attempted in patients with history of non-IgE-mediated systemic reactions such as Guillain–Barré syndrome, peripheral neuritis, haematological and renal complications. Investigations.  Skin prick tests (SPT) are the first-line investigation and are carried out at a concentration of 0–100 µg/ml of standardized venom extract [39].

© 2009 Wiley-Liss, Inc. Microsurgery, 2010. “
“Recidivating pressure sores are a frequent complication in meningomyelocele patients because of their limitation in motility and their scarce ability

to monitor the pressure applied on insensate areas while seated. We report the utilization of the sensate pedicled anterolateral thigh perforator flap for reconstruction of ischiatic sores in meningomyelocele patients. Between May 2011 and September 2013, five patients underwent transfer of a sensate pedicled anterolateral thigh flap, by an intermuscular passageway through the upper thigh, to reach the ischial defect. Flap was properly harvested from the thigh after assessment of the lateral cutaneous femoral nerve sensitive area with the Pressure-Specified Sensory Device. In all cases the flap reached https://www.selleckchem.com/products/obeticholic-acid.html the ischial defect harmlessly, healing was uneventful with no immediate nor late complications. Each patient showed persistence of sensitivity at the reconstructed area and no recurrent ischiatic sore was observed at mean follow-up of 26.4 months. The sensate

pedicled anterolateral thigh flap is a valuable solution for coverage of recurrent ischial sores in meningomyelocele patients, in which pressure consciousness is fundamental. The intermuscular passageway allows to reduce the distance between flap’s vascular pedicle origin and the ischial defect, hence to use the more reliable skin from the middle third of the anterolateral thigh. © 2014 Wiley Periodicals, Inc. Microsurgery, 2014. “
“Background: BGB324 supplier No consensus exists among microsurgeons regarding the role of intravenous (IV) heparin in digital replantation/revascularization. The current experience of the Provincial Replantation Center in Quebec was reviewed over a 4-year period. Methods:

An initial retrospective review of all revascularized or reimplanted digits at our Replantation Center from April 2004 to April 2006 was conducted. Then, data of all patients treated at our center from January 08 to September Acyl CoA dehydrogenase 08 were prospectively collected. The two cohorts were compared with regards to demographics, injury characteristics, postoperative thromboprophylaxis medication as well as complication and success rates. Proportions were compared using χ2 tests/Fisher’s exact tests. Multivariate analysis was conducted with logistic regression. Results: 175 digits were treated from April 2004 to April 2006, including 104 revascularizations and 71 amputations. IV heparin was used in 35.1% of the cases and was associated with a 3.59-fold (95% CI, 1.55–8.31) increase risk of developing a complication compared with cases where heparin was not used (P = 0.001). In 2008, 106 digits were treated. IV heparin was used in 14.6% of the cases and was not significantly associated with a higher complication rate compared with cases where heparin was not used (P = 0.612). Both cohorts’ success rates were very similar (P = 0.557).

05) (Table 1). The mean pre-operative QOL was 4.3 ± 0.7, while it was 1.15 ± 0.8 at 3 months and 1.3 ± 0.6 at 12 months postoperatively, which was a statistically significant difference between pre- and postoperatively at both 3 months (P < 0.01) and 12 months (P < 0.01), but the difference between 3 and 12 months

postoperatively was not statistically significant (P < 0.05) (Table 1). The mean pre-operative RU was 85.6 ± 6.0 mL while it was 25.6 ± 8.5 mL at 3 months and 27.1 ± 8.5 mL at 12 months postoperatively. The difference between pre-operative RU and postoperative both at 3 months (P < 0.01) and 12 months (P < 0.01), but the difference PLX4032 clinical trial between 3 and 12 months postoperatively was not statistically significant (P < 0.05) buy BGJ398 (Table 1). According to the result of statistical analysis, which was summarized in Table 1, the patients become asymptomatic. Maximum urinary flow rate rose up to its normal range, good quality of life ensued, and no significant post-voiding residual urine appeared. This result indicates that TV pedicle flap urethroplasty is a safe and successful

procedure for patients with anterior urethral stricture. There were few changes in clinical parameters between 3 and 12 months postoperatively, but the differences were not statistically significant. An early postoperative complication was one case of wound infection and subsequent wound dehiscence in tabularized technique and also one case of hematoma formation in ventral onlay technique. Wound infection was resolved by 2-weeks of antibiotic therapy and the hematoma was drained. In one patient on the tabularized technique, re-stricture developed, while in the onlay technique, one case of urethro-cutaneous occurred.

Both of them were considered failed cases. There was no other complication like penile curvature (chordee) in our series. The total success rate in our study was 86.6% (13/15). Glutamate dehydrogenase There was no statistically significant difference between success rate of tabularized and ventral onlay technique. A great variety of tissues from the genital and extra genital area have been tried both experimentally and clinically for a flap or free graft. These include the fasciocutaneous component of the penis, bucal mucosa graft, vesicle mucosa, small intestinal sub-mucosa and peritoneum.[4] Besides that, several surgical techniques have been launched to find an ideal substitute for the urethra, but it seems that the ideal graft or flap has not been identified yet. Based upon many previous experimental studies, we clinically evaluated the feasibility and usefulness of tunica vaginalis pedicle flap for reconstruction of anterior urethral stricture in the form of ventral onlay and tabularized techniques. Our sample comprised 15 adult men with bulbo-penile acquired urethral stricture, of which nine underwent TV-ventral onlay and six underwent TV-tubularized urethroplasty.

If an entire exon is deleted without the presence of a mutation in the bordering exons, a splice-site mutation may be present in the bordering introns in the genomic DNA. This, too, must be analysed in NCF1-specific PCR amplicons. For protocols see [29, 30]. Some investigators apply screening for a mutation in a PCR product to select the fragment to be sequenced. For this purpose, single-strand conformation polymorphism analysis [31], denaturing high-pressure liquid chromatography [32] or high-resolution melting analysis [33] can be used. Single-strand conformation polymorphism

(SSCP) is based on the difference in electrophoresis profile between denatured patients’ PCR products and wild-type PCR Selleck Metformin products in a polyacrylamide gel. PCR products with an aberrant migration pattern are then sequenced. Denaturing high-pressure liquid chromatography (DHPLC) is based on heteroduplex formation between a PCR product from a patient with a wild-type PCR product. In case the two PCR products differ, the elution profile of the heteroduplex over

a column will differ from the profile seen with a wild-type homoduplex. Such PCR products are then sequenced. High-resolution melting analysis is based on the difference in melting curves between hetero- and homoduplexes. However, as BMN673 a lack of aberrant signal does not guarantee a wild-type sequence in the patient’s PCR product in any of these methods, such screening assays are not generally applied. Splice-site mutations found in genomic DNA should be confirmed for their effect on mRNA splicing by analysing the lack of one or more exons in the cDNA of the patient. Also, the presence of large deletions, usually based on the lack of PCR product formation, should be confirmed by an independent assay, such Venetoclax supplier as multiplex ligase-dependent probe amplification

[34] or array comparative genomic hybridization [35]. Restriction fragment length polymorphism (RFLP) analysis is also possible, but this technique is tedious, requires a great deal of freshly purified genomic DNA and does not always lead to unequivocal results. Multiplex ligase-dependent probe amplification (MLPA), with a set of probes annealing at different positions, analyses which parts of a gene or gene-surrounding sequences are still present. In array comparative genomic hybridization (ACGH), DNA from a test sample and from a normal reference sample are labelled differently with fluorescent dyes and are then hybridized to a set of probes on a glass slide. The ratio of the fluorescence intensity of the test DNA to that of the reference DNA is then calculated, to measure the copy number changes for a particular gene or gene fragment.

002). Furthermore, 36.4% of the C-allele carriers and none of the patients with the TT genotype belonged to group B (P = 0.005). C-allele Wnt tumor carriers also had a worse kidney survival in the Kaplan–Meier analysis (P = 0.027). Conclusion:  Our results indicate that aldosterone synthase gene C-344T polymorphism not only acts as a risk factor for the development of FSGS, but also may influence its pathologic appearance

and could serve as a marker of disease progression. “
“Autosomal dominant polycystic kidney disease (ADPKD) is a monogenetic disorder that leads to kidney failure. Our aim was to undertake a meta-analysis of randomized trials of interventions that have been hypothesized to reduce the progression of total kidney volume (TKV) and renal function in ADPKD. Relevant trials were identified, and outcomes were: change in TKV, total cyst volume (TCV), renal function and adverse events. Meta-analysis used random effects, with results expressed as mean difference and risk ratio both with 95% confidence intervals (CI). Eleven trials (2262 patients) were included. Compared with placebo, Target of Rapamycin complex 1 (TORC1) inhibitors (5 trials, n = 619), showed no significant change in TKV (P = 0.21), TCV (P = 0.06) or eGFR (P = 0.22). Somatostatin analogues (3 trials, n = 157) reduced TKV by 9% (95% CI −10.33 to −7.58%) but did not alter eGFR. The vasopressin receptor

antagonist (n = 1455) attenuated TKV increase to 3%/year (95% CI −3.48 to −2.52) and slowed kidney function JNK pathway inhibitors decline over a 3-year period. A single trial (n = 41) of eicosapentaenoic acid did not alter the progression of either TKV (P = 0.9) or renal dysfunction (P = 0.78). Adverse events were significant for interventions in all trials compared with placebo. These data suggest

that somatostatin analogues and vasopressin receptor antagonists attenuate TKV increase. The neutral effects of TORC1 inhibitors on TKV could be true, or due to heterogeneity in study population, drug efficacy and follow-up duration. In the future, further well-designed and powered trials of longer duration using new biomarkers or therapeutic agents with better tolerance are required. “
“We herein describe the unique case of a 59-year-old man who underwent living kidney transplantation for IgA nephropathy (IgAN) and developed progressive kidney failure associated with the appearance of proliferative glomerulonephritis. of An early protocol biopsy revealed recurrent IgAN with mesangial IgA2 deposits restricted to a single immunoglobulin λ light-chain isotype. Despite treatment with tonsillectomy and rituximab, the patient eventually lost his allograft 31 months after transplantation. Serum electrophoresis showed a monoclonal IgA pattern. This case might share common pathological characteristics with the newly described entity referred to as proliferative glomerulonephritis with monoclonal IgG deposits. A 59-year-old Japanese man developed end-stage renal disease secondary to IgA nephropathy (IgAN).

An interesting feature is the low CD62L expression by mobilized PCs. CD62L plays an important role in leucocyte–endothelial cell interaction. It is essential to mediate lymphocyte adhesion and transmigration into the lymph nodes from high endothelial venules to the parenchyma, and also contributes to the recruitment of leucocytes from the blood to areas of inflammation.25 CD62L is highly expressed by circulating PCs

detected in steady-state conditions or 7 days after TT vaccination,13–15 while it is absent on PCs from the BM, spleen or tonsil.14,15 CD62L is also expressed by newly generated PCs in vitro. 20 The role of CD62L in PC migration into the BM is not known, and the homing of mobilized PCs in the BM remains to be demonstrated. The check details lack of CD62L expression by mobilized PCs suggests that these

PCs could originate from AZD1152 HQPA the BM or tissue PCs that are induced to recirculate, and they do not correspond to newly generated PCs. These findings, together with the relatively high expression of KI-67 found for mobilized PCs, indicate that these cells are not quiescent and that the mobilization process of tissue PCs into the PB could require activation of BM/tissue PCs and their entry into the G1 cell cycle phase. The overall number of PCs in a healthy individual has been estimated to be around 109.1 These PCs may survive for decades at least and are responsible for the long-term humoral memory. Based on these calculations, the number of infused PCs would represent around one-thirtieth of the overall PC count in an adult. It is interesting to consider that these cells can home to the BM and other tissues and contribute to maintain some of the donor’s humoral memory in the grafted patient. Calpain This work was supported by grants from the Ligue Nationale Contre le Cancer (équipe labellisée 2009), Paris, France, from INCA (n° RPT09001FFA), and from MSCNET European strep (N°E06005FF).

Cytometry analyses were run on the cytometry platform of the Institute of Research in Biotherapy (http://irb.montp.inserm.fr/en/index.php?page=Plateau&IdEquipe=3, Montpellier Rio Imaging). The authors report no potential conflicts of interest. AC contributed to the carrying out of the experiments, the design of the research, and the writing of the paper. MPA and AO contributed to the writing of the paper. ML contributed to the carrying out of the experiments. TK, ZYL and JFR provided the donor samples. BK contributed to the design of the research and the writing of the paper. “
“Commercially available inactivated vaccines against porcine circovirus type 2 (PCV2) have been shown to be effective in reducing PCV2 viremia. Live-attenuated, orally administered vaccines are widely used in the swine industry for several pathogens because of their ease of use yet they are not currently available for PCV2 and efficacy.

The cells on coverslips were infected with DsRed- and/or EGFP-tagged adenoviruses, at moi of 100, in the presence or absence of 0.5–1 μmol/L MG-132 (Sigma) or 5 mmol/L 3-methyladenine (3MA; Sigma). After 48 h, the cells were fixed with 4% paraformaldehyde in PBS, permeabilized with Palbociclib 100% methanol, washed with PBS, and immunostained overnight at 4°C with the following primary antibodies at 1:200 dilutions; mouse monoclonal TuJ1 (R&D Systems, Minneapolis, MN, USA), mouse-O4 (R&D), mouse anti-p62 (BD Biosciences, San Jose, CA, USA), rabbit anti-TDP-43 C-terminus (Cosmo Bio), rabbit anti-FUS (Sigma), rabbit anti-GFAP (DAKO,

Glostrup, Denmark), rabbit anti-ubiquitin (DAKO) and rabbit anti-choline acetyltransferase (ChAT;

Millipore, Billerica, MA, USA). The cells were then incubated with Alexa Fluor 350 or 488-conjugated goat anti-rabbit or anti-mouse antibodies (Invitrogen) at 1:400 dilutions for 1 h at room temperature, followed by incubation for 15 min with 2 μg/mL Hoechst 33342 (Invitrogen). After washings, coverslips were mounted on glass slides with Gelvatol (20% glycerol/10% polyvinyl alcohol in 0.1 mol/L Tris CB-839 molecular weight buffer, pH 8.0). Immunostained cells were examined under an Olympus AX80TR microscope equipped with DP70 CCD camera. The experimental protocols were approved by the Animal Care and Use Committee of the Tokyo Metropolitan Institute of Medical Science. Adult Fischer 344 male rats (8–12 weeks old, 150–200 g) were anesthetized with intraperitoneal injection of pentobarbital sodium (40 mg/kg). Under a dissecting

microscope, the right facial nerve was exposed and 10 μL solution in total of recombinant adenovirus(es) (1 × 108 plaque-forming units (pfu) each for single and combined injection) was slowly oxyclozanide injected into three facial nerve branches using a 33G microsyringe (Hamilton, Reno, NV, USA). The virus suspension was mixed with Evans blue (0.01% final; Sigma) to confirm visually that the injection was successfully performed. The wounds were covered with a small piece of gelatin sponge (Gelfoam; Pharmacia Upjohn, Bridgewater, NJ, USA) and suture closed, and the animals were killed at 3–7 days post-operation as described below. Rats were anesthetized with a lethal dose of pentobarbital sodium and transcardially perfused with 0.1 mol/L phosphate buffer, pH 7.4 (PB) followed by 4% paraformaldehyde in 0.1 mol/L PB. The brain stem tissue containing facial nuclei and their intramedullary nerve tracts was dissected and immersion fixed in the same fixative as described.[24] The brain stem tissues were cryoprotected in 30% sucrose in 0.1 mol/L PB and serial transverse sections (15 μm thickness) were made by cryostat.

In human renal biopsy with DN, the levels of decreased Sirt1 in PT or Pods and increased Claudin-1 in Pods were correlated with proteinuria levels. Conclusion: Our results (Hasegawa K, Nature Medicine 2013) suggest that Sirt1 in PTs protects against diabetic see more albuminuria by maintaining

NMN around Pods, thus influencing glomerular function. Although tubulo-glomerular feedback has been previously reported, ours is the first description of a proximal tubular substance (NMN) that communicates with podocytes as a key mediator of intracellular crosstalk. KIM SU-MI, LEE YU-HO, KIM SE-YUN, KIM YANG-GYUN, JEONG KYUNG-HWAN, LEE SANG-HO, LEE TAE-WON, IHM CHUN-GYOO, MOON JU-YOUNG Division of Nephrology, Department of Internal Medicine1, Kyung Hee University, College of Medicine Background: Mycophenolate mofetil (MMF) is a commonly used anti-lymphocyte drug with immunosuppressive/anti-inflammatory properties and has been used MI-503 chemical structure in recent years to prevent glomerular injury. It is a reversible inhibitor of inosine monophosphate dehydrogenase in purine biosynthesis

which is necessary for the growth of T cells proliferation. Proinflammatory T helper 1 (Th1) and T helper 17 (Th17) cell subsets have been associated with the pathogenesis of multiple autoimmune diseases. We already reported that CD4+ T cell is increased in diabetic kidney. However, the role of Th1 and Th17 cells PD184352 (CI-1040) in the development and progression of diabetic nephroapathy remains largely unknown. In this study, we examined the hypothesis

that MMF attenuates diabetic kidney injury by depression of renal T-cell proliferation and related cytokine. Methods: Streptozotocin (STZ)-induced diabetic mice were treated with 30 mg/kg daily MMF during 3 to 20 weeks of diet. Body weight, kidney weight, fasting blood glucose, and glycosylated hemoglobin (HbA1c) were measured at the time of sacrifice. Twelve-hour urinary albumin-creatinine ratio and HbA1c were measured by immunoassay. To assess renal tissue damage, PAS-stained kidney sections Kidney sections were stained with PAS and evaluated for the presence of mesangial matrix expansion. IFN-γ and IL-17 production of kidney infiltration CD4+ T cells was investigated in kidney mononuclear cell by flow cytometry. Results: The HbA1c level were equally elevated with or without MMF in STZ-induced mice. Twelve-hour urinary albumin excretion increased markedly in diabetic mice, but decreased urinary albumin excretion in MMF-treated diabetic mice. Blood neutrophil and WBC counts showed mild reduction by MMF-treatment. In flow cytometry of kidney mononuclear cell, diabetic mice showed increase of IFN-γ for Th1 cells and IL-17 for Th17 cells from 8 weeks. MMF reduced the production of a number of T-cell cytokines as IFN-γ for Th1 cells and IL-17 for Th17 cells at 8 weeks.

v.) rabbit IgG administration (IVIgG) on allergic airway inflammation and lung antigen-presenting cells (APCs) in a murine model of ovalbumin (OVA) sensitization and challenge. In OVA-challenged mice, IVIgG attenuated airway eosinophilia, airway hyperresponsiveness and goblet cell hyperplasia and also inhibited the local T helper type (Th) 2 cytokine levels. Additionally, IVIgG attenuated the proliferation of OVA-specific CD4+ T cells transplanted into OVA-challenged mice. Ex PD-0332991 price vivo co-culture with OVA-specific CD4+ cells and lung CD11c+ APCs from mice with IVIgG revealed the attenuated transcription level of Th2 cytokines,

suggesting an inhibitory effect of IVIgG on CD11c+ APCs to induce Th2 response. Next, to analyse the effects on Fcγ receptor IIb and dendritic cells (DCs), asthmatic features

in Fcγ receptor IIb-deficient mice were analysed. IVIgG failed to attenuate airway eosinophilia, airway inflammation and goblet cell hyperplasia. However, the lacking effects of IVIgG on airway eosinophilia in Fcγ receptor IIb deficiency were restored by i.v. transplantation of wild-type bone marrow-derived CD11c+ DCs. These results demonstrate that IVIgG attenuates asthmatic features and the function of lung CD11c+ DCs via Fcγ receptor IIb in see more allergic airway inflammation. Targeting Fc portions of IgG and Fcγ receptor IIb on CD11c+ DCs in allergic asthma is a promising therapeutic strategy. Bronchial asthma is a disorder of the conducting airways characterized by variable airflow obstruction, but is also a chronic inflammatory disease of the airway associated with an immune response to inhaled antigens, which

leads to airway infiltration of eosinophils and mast cells, goblet cell hyperplasia and airway hyperresponsiveness (AHR). These pathophysiological GBA3 features are induced by T helper type (Th)2 proliferation and production of Th2 cytokines, such as interleukin (IL)-4, IL-5 and IL-13 [1]. Anti-inflammatory drugs, primarily corticosteroids, comprise the conventional treatment for chronic Th2 airway inflammation. The current anti-inflammation strategies to manage bronchial asthma have limited clinical efficacy for some patients. Immunoglobulins (Igs) and Fc receptors (FcRs) play important roles in bronchial asthma pathogenesis. FcRs are expressed on many kinds of immune cells and control the cellular functions. Among Igs, IgE plays a crucial role in the pathogenesis of asthma by binding airborne inhalant allergen to activate various cellular inflammatory reactions of immune cells through FcεRI. Anti-IgE therapy, one of the controllers to manage bronchial asthma, reduces the free IgE available to activate effector cells [2]. In contrast, IgG reportedly has immunomodulatory effects on the immune response to common inhalant allergens. Immunotherapy by allergen vaccination is accompanied by an increase in allergen-specific IgG titres [3].