The word “Jeevandan” means “to donate life ” We present our exper

The word “Jeevandan” means “to donate life.” We present our experience of deceased donor transplantation program initiated by government of Andhra Pradesh, selleck chemicals llc India. Results: Jeevandan program practically came into force from 1st January 2013 since then, there were 40 cadaveric donations. Male Donors were 32 and female 8. The mean age was 37.5 years (range 8 to 72). Most common Blood group was B positive in 16 (40%) donors followed by O positive in 12 (30%), O negative in one (2.5%), A positive in 8 (20%) donors, and AB positive was seen in only 3 (7.5%) donors. Total 180 organs and tissues were retrieved from

40 deceased donors; 75 kidneys, 34 livers, 33 heart valves 34 corneas and 2 lung and 2 Hearts. Total deceased donor renal transplantations done during this period were 75. Out of 40 donors, kidneys were not utilized

from 2 donors; as one donor had chronic kidney disease with serum creatinine of 4.5 mg/dl and other donor was 72 year old female with hypertension, diabetic and diabetic nephropathy. One kidney was wasted because of positive cross match. Mean age of renal recipients was 40.36 years (range 13 to 64). There were 18 females and 57 males, female to male ratio being 1: 3.15. Mean follow of renal transplant recipients was 5.8 months. Eighteen patients (24%) had delayed graft function. One (1.72%) patient underwent graft nephrectomy due to candida fungal aneurysm of the graft. Two patients (2.66%) patient developed humeral mediated rejection. Mortality rate selleck compound was 8%. Conclusion: Every country should have a deceased donor transplantation program. ALAM MUHAMMAD RAFIQUL, WAHEED S Bangabandhu Sheikh Mujib Medical University Introduction: Estimation renal of size provide clue to diagnosis & prognosis of different kidney diseases.

Renal size estimation by sonography is a convenient method. Observer variation in this measurement is an important factor. Therefore; it obviously demands measurement of live kidney size in our ethnicity and it’s comparison with ultrasound and other methods for estimating kidney size. Materials & Methods: A total of fifty prospective living related kidney donors, male (19) & female (31) were enrolled. Loperamide The study was carried out to compare the per operative length of the harvested kidney with the length of that particular kidney measured by USG and CT IVU methods and kidney lengths obtained were correlated with some parameters of the donor like age, sex, height, body weight and body surface area, split GFR, CCr, e GFR (C&G) and GFR by DTPA. Results: The mean of age, height, weight, surface area, CCr, e GFR, DTPA GFR was 38.98,156.54 cm, 52.75 kg, 1.50 m2, 84.25 ml/min, 69.88 ml/min/ m2, 90.38 ml/min/m2 respectively. The mean length of right kidney (male) was 10.35 cm, 9.78 cm, 10.

Presentation of exogenous antigen

by both non-classical M

Presentation of exogenous antigen

by both non-classical MHC class I molecules and classical MHC class II molecules requires antigen entry into Kinase Inhibitor Library cell assay the endosomal pathway 39, 40. In agreement with this, we demonstrated that an endosomal pathway operates in the presentation of TCR-peptides associated with I-Au and Qa-1 molecules to CD4+ and CD8αα+TCRαβ+ Treg, respectively (Fig. 3 and 24). We have yet to determine whether CD4+ and CD8αα+TCRαβ+ Treg are primed by the same DC. We do, however, think this is the case due to the shared endosomal pathway and for the following reasons: (i) DC engulf Vβ8.2+ apoptotic T cells containing both the cognate CD4+ and CD8αα+TCRαβ+ Treg antigenic determinants; (ii) DC are adept at presenting antigen in the context of both MHC class II and non-classical class I molecules; (iii) CD4+ T cells can license selleck kinase inhibitor DC, e.g. by CD40L-CD40 interactions, to stimulate a CD8+ T-cell response 41 and (iv) CD4+ T cells may provide help through the secretion of cytokines that act directly on proximal CD8+ T cells 42. We have shown that injection of DC pulsed with Vβ8.2+ apoptotic T cells or TCR peptide B5 prime CD4+ Treg in vivo (Fig. 4) and that DC loaded with B5 can protect from EAE disease (Fig. 5). Data presented here and in

other studies demonstrate that DC are the most efficacious APC for inducing optimal T-cell responses 43. DC can migrate to lymphoid organs, process and present antigens from multiple sources by both MHC class I and class II pathways, cross-present non-replicating antigens and be manipulated to induce immunogenic or tolerogenic responses. However, to date immunotherapeutic studies that have attempted to harness the immuno-modulating ability of the DC, either by targeting antigens to the DC in vivo or by adoptive transfer

of antigen-loaded DC, have demonstrated minimal clinical efficacy 44. One major hindrance has been the lack of knowledge of the specific antigen targets. Here we have delineated the mechanism by which defined antigens are presented to a characterized CD4+ Treg population. Our data clearly show that disease-causing CD4+ T cells can be used to pulse DC’s for efficient in vivo priming of appropriate CD4+ as well as CD8+ Treg populations Tryptophan synthase and subsequent regulation of autoimmune disease. Thus, in this defined system we have an excellent opportunity to study the optimal way to manipulate DC therapy to induce optimal priming of the T cells involved in regulation of an autoimmune disease. In addition, our data suggest a DC-based immune intervention strategy for the induction of negative feedback regulation of T-cell-mediated inflammatory autoimmune disease. B10.PL and PL/J H-2u mice were purchased from Jackson Laboratory (Bar Harbor, ME). CD8−/− PL/J mice were kindly provided by Dr. Tak Mak 45.

The eight strains isolated from Jiangsu Province in 1998 were als

The eight strains isolated from Jiangsu Province in 1998 were also included (six from patients and two from diseased pigs) (Table 1) (9, 15). All of the strains were screened using PCR targeting virulence-associated

genes including MRP (mrp), suilysin (sly) and EF (epf) (16). All of the isolates were also characterized using single enzyme PFGE with SmaI (9) and a MLST scheme (11). The complete genome sequence of five S. suis serotype 2 strains including GZ1 (ST1) (8), SC84 (ST7, NC_012924), 05ZYH33 (ST7) (17), 98HAH12 (ST7) (17), and P1/7 (ST1) (http://www.sanger.ac.uk) were analyzed for potential VNTR loci using TRF, (version 2.02) (18) and the ABT-199 order Tandem Repeat Database (http://minisatellites.u-psud.fr/) using alignment parameters as follows: two matches, three mismatches, and five indels

where 50 was the minimum alignment score; 500 bp was the maximum array size of the repeat unit. Where multiple repeat patterns existed in a given locus, the repetitive unit pattern with the highest match rate was selected. To avoid missing a locus where only one copy was in a given sequenced strain whereas multiple repeat copies occur in other strains, Y-27632 datasheet the TRF output generated from the P1/7, GZ1, SC84, 05ZYH33 and 98HAH12 genomes was compared. Primer Premier 5.0 was used to design the PCR primers targeting the VNTR loci within the flanking regions. Overlapping or adjoining tandem repeats were co-amplified with a single set of primers (19). Strains were cultured on sheep Columbia blood agar plates at 37°C in 5% CO2

for 24 hr. A single isolated colony was inoculated into 5 ml Todd-Hewitt broth and incubated overnight. Total genomic DNA was isolated using QiaAmp DNA isolation columns (Qiagen Gene, Beijing, China) and following the manufacturer’s instructions for Gram-positive bacteria. Standard PCR was performed per the manufacturer’s directions using Taq DNA polymerase (TaKaRa, Beijing, China) in 25 μl reaction mixtures: 2.5 μl buffer (10×), 5 U Taq DNA Inositol monophosphatase 1 polymerase, 200 μM each deoxynucleoside triphosphate, 1 μl bacteria genome DNA (10 ng/μl), 0.5 μM each oligonucleotide primer, and RNase-free water. The PCR reaction was performed using a thermal cycle PTC-200 DNA Engine (MJ Search, Beijing, China). The PCR regimen consisted of an initial denaturing at 95°C for 10 min followed by 30 cycles of amplification: 95°C for 1 min, annealing temperature for 1 min, and extension at 72°C for 1 min; with a final extension at 72°C for 10 min. The amplified products (1.5–2.5 μl) were resolved using electrophoresis on a horizontal 1.5% agarose gel (Amplisize, Bio-Rad, Hercules, CA, USA) at a voltage of 6 V/cm for approximately 4 hr using 0.5×TBE buffer (10×TBE is 890 mM Tris base, 890 mM Boric acid, and 20 mM EDTA; pH 8.0). The gels were stained with ethidium bromide (0.

A visiting palliative care specialist from St George Hospital pro

A visiting palliative care specialist from St George Hospital provides an

outreach service as well as phone advice, support and ongoing education to up skill local practitioners and trainees. This team approach Sotrastaurin in vitro has improved the services and outcomes for patients on non-dialysis pathways but also those on a dialysis pathway as an unintended ripple effect with different approaches to symptom control. The role of the supportive care nurse in this model is critical to the success of this model promoting a wider referral base especially from dialysis nurses and Allied health. The caring physician’s may not always be aware of the iceberg of symptoms that are very apparent to the dialysis staff that care for these patients during the long hours of dialysis. A similar model is being set up in Western Australia linking into existing palliative care services if available.[11] Options for certification in renal supportive care for nurses and allied health professionals and ongoing education in renal supportive care need to be explored with the Renal Society Selleck PF2341066 of Australasia (RSA). Robyn Langham General practitioner are important and should be involved in decision

making and advanced care planning (ACP) for patients with advanced kidney disease. Advanced kidney disease has a biphasic nature of life trajectory. No treatment does not mean no dialysis for the patient with chronic kidney disease (CKD) – CKD care and terminal phase care. For patients and their families undergoing renal supportive care, their primary care physician is an integral member of the multidisciplinary team. From a generic palliative care viewpoint, the Gold Standards Framework[1] outlines the importance of the general practitioner in palliative Immune system care, the importance of enhancing knowledge and understanding of palliative care and underlines the need for effective communication, coordination and continuity of care. It emphasizes

the importance of case identification, holistic assessment, care planning, individual case discussions and case management by a multidisciplinary team as well as family and carer’s assessment and support. These principles can be directly applied when evaluating the role of the primary care physician in renal supportive care. Recent data from the AIHW indicates that for every new case of end-stage kidney disease (ESKD) treated with renal replacement therapy (RRT – dialysis or transplantation), there is one that is not, although the vast majority of those not treated are elderly. Furthermore, the rate of non-RRT treatment varies greatly with age, with RRT rates dropping progressively over the age of 65, with only about one-tenth of those aged 80 years or over receiving dialysis or transplant.

A total of 2371 men and 731 women were analyzed In this study, M

A total of 2371 men and 731 women were analyzed. In this study, MS was defined according to the International Diabetes Federation (IDF) consensus of 2005, and LUTS was accessed with IPSS. Contrary to the previous results, the authors did not find a significant association between MS and the presence or severity of LUTS in either men or women. On multiple linear regression, the presence of MS was not associated with obstructive, irritative or total IPSS. Therefore, they suggested that MS is selleck screening library not independently associated with LUTS.19 Between 2005 and 2007, we performed an epidemiological study investigating LUTS in diabetic women. A total of 518 women with type 2 diabetes

who visited the Department of Metabolism see more at National Taiwan University Hospital (NTUH) were included in the study.20 According to the NCEP ATP III metabolic diagnostic standards, we divided the diabetic women into control and study groups. The control group had diabetes without MS (272 cases) and the study group had diabetes with MS (246 cases).

We evaluated LUTS of these two groups using the International Prostate Symptom Score (IPSS) questionnaire. In summary, diabetic women with a diagnosis of MS had more severe storage symptoms (4.8 ± 0.3 versus 3.7 ± 0.3, P = 0.025), such as urgency (2.0 ± 0.2 versus 1.1 ± 0.1, P < 0.001) and nocturia (2.1 ± 0.1 versus 1.6 ± 0.1, P < 0.001). Obstructive symptoms were more severe in women in the study group as well, but with a borderline statistical significance (3.8 ± 0.5 versus 2.4 ± 0.4, P = 0.052). In terms of the total IPSS, the study group had a significantly higher score than the control group (9.1 ± 0.7 versus 6.5 ± 0.6, P = 0.003) (Fig. 1). The prevalence of LUTS as defined by total IPSS ≱ 8 was also higher in the study group (44% versus 30%, P = 0.022). We further divided the study group women into three subgroups based on the number of MS risk factors (Fig. 2), and we discovered that in diabetic women, the total IPSS and the odds ratio

for LUTS increased as the number of MS factors increased. Oxalosuccinic acid However, the result of multivariate analysis indicated that diabetic peripheral neuropathy, but not MS, was an independent factor for LUTS in diabetic women. What were the reasons for this discrepancy? We suggest that diabetes-related complications, such as peripheral neuropathy, is the main predictor of LUT dysfunction in women with type 2 diabetes; but the risk is modified and compounded by the presence of MS. To date, the relationship between MS and LUTS remains controversial. According to our own experience, the development of LUTS is multifactorial, MS alone cannot explain the full spectrum of LUTS. Future works should focus on preventing risk factors for MS, thus reducing its associated morbidities and diminishing the medical expenses.

46 Nakayama et al 47 provided evidence for a beneficial effect of

46 Nakayama et al.47 provided evidence for a beneficial effect of immune cells on early events of embryo implantation by showing that human peripheral blood leukocytes (PBL) from pregnant mothers enhanced murine embryo spreading and invasion in vitro. In addition, co-culture of PBMC isolated from pregnant women with BeWo-cells (i.e., a trophoblast cell line) enhanced their ability to invade into matrigel compared with PBMC isolated

from the secretory phase of the menstrual cycle.48 This effect occurred with the cells isolated on either side of a 0.8 -μm membrane, suggesting the effect was induced by a soluble factor secreted by the PBMC. This factor could, in fact, be CG which was shown to be produced and secreted by PBMC during early pregnancy in women.49 Moreover, Kosaka et al.50 showed PBL promoted attachment of BeWo-cell spheroids to endometrial cells derived from human uteri in the late proliferative click here and GDC-0449 ic50 early secretory phases. They suggested that PBL may be able to induce endometrial

cells to become ‘receptive’ to embryo implantation. In agreement, Yoshioka et al.51 found that hCG-primed PBMC, in conjunction with freshly prepared PBMC, increased pregnancy rates in women when the PBMC were administered into the uterine lumen 1 day prior to blastocyst transfer. Collectively, these studies highlight how the immune and endocrine system may coordinate events for the establishment and maintenance of pregnancy, and how conceptus signals responsible for rescuing CL function may also play a role in counter-balancing the immunosuppressive effects of progesterone. Surprisingly, there have been relatively few studies examining the effects of hCG on peripheral immune cell gene expression, and no reports

of global transcriptional profiling experiments on mafosfamide hCG-stimulated immune cells. In the early to mid-1990s, several studies revealed potential similarities between CG and the ruminant type I IFN family to which IFN-τ belongs. In those reports, the β-subunit of CG was purported to possess antiviral activity (characteristic of interferons) against HIV.52–54 However, subsequent studies revealed that this activity resulted from contamination of the preparation by lysozyme and RNAses present in the urine of pregnant women from which the CG was purified.55 These results are consistent with those of Gunn et al.56 who were unable to detect antiviral activity in media conditioned by culture with peri-implantation stage human embryos, even if the embryos were producing detectable amounts of CG. However, there is ample evidence that the human placenta produces IFN during gestation that alters local immune cell function.57 For example, interferon-stimulated gene 15 (ISG15) is induced during early pregnancy in the endometrium of the baboon and human.

When the target tooth was missing, the second molar in the same s

When the target tooth was missing, the second molar in the same side or the first incisor in the opposite side was examined. The deepest PPD was recorded for each tooth. Periodontal disease was defined as positive if a woman had at least one tooth with a PPD of 3.5 mm or deeper. Among the 1157 women, 131 cases of periodontal disease were identified using this definition. The 1026 remaining participants were eligible to serve as control subjects, but seven women were excluded because of missing

data on the factors under study; thus, 1019 women were classified as control subjects. In the baseline survey, each participant filled out a questionnaire and mailed it to the data management H 89 in vitro centre. Research technicians completed missing or illogical data by telephone interview. The questionnaire in the baseline survey included questions about smoking habits, household income, education, toothbrushing frequency and use of an interdental brush.

A history of smoking was defined as having smoked at least once per day for at least 1 year. Research technicians or subjects themselves collected buccal specimens with BuccalAmp swabs (Epicenter BioTechnologies, Madison, WI, USA). Genomic see more DNA was extracted using a QIAmp DNA mini kit (Qiagen, Inc., Valencia, CA, USA). Genotyping of VDR SNPs was performed using TaqMan SNP Genotyping Assays on a StepOnePlus machine (Applied Biosystems, Foster City, CA, USA), according to the manufacturer’s instructions. Departures from Hardy–Weinberg equilibrium were tested among the control subjects using the Chi-square test. Linkage disequilibrium was examined using Haploview software version 4.2 (Broad Institute, Cambridge, MA, USA) [23]. Estimations of crude odds ratios (ORs) and 95% confidence intervals (CIs) for periodontal disease associated with the SNPs under

study CYTH4 were made by means of logistic regression analysis, with the reference category being the homozygote of the major allele. Multiple logistic regression analysis was used to control for age at oral examination, region of residence, education, smoking, toothbrushing frequency and use of interdental brush. The statistical power calculation was performed using QUANTO version 1.2 [24]. Haplotypes and their frequencies were inferred according to the expectation maximization algorithm. For differences in haplotype frequency between the cases and control groups, crude ORs and 95% CIs were estimated based on the frequency of each haplotype relative to all other haplotypes combined. We examined multiplicative and additive interactions between the SNPs under study and smoking with regard to the risk of periodontal disease. The multiplicative interaction was estimated by introducing a multiplicative term into a multiple logistic regression model.

9a,b) in a STIM1-dependent manner and by CD28-dependent store-ind

9a,b) in a STIM1-dependent manner and by CD28-dependent store-independent activation of Ca2+ entry, potentially in a STIM2/ORAI1 or ORAI3-dependent manner. The CD28-dependent Ca2+ entry can occur in the context of the IS formation. If only CD28 is expressed, we would therefore not expect differences in

Ca2+ signals between CD80 or CD86 costimulation because CD28 is recruited to the IS independent of the type of costimulation (Fig. 9a). This is the case in Jurkat E6-1 and naïve primary T cells. However, if both CD28 and CTLA-4 are present at high concentrations, as in the case of effector T cells, it is expected that CD80 should preferentially bind to CTLA-4 and not so much to CD28, with the opposite being true for CD86.37 Therefore, CD86 should enhance CD28 recruitment to the IS and CD80 should inhibit CD28 recruitment by recruiting CTLA-4 instead. Through an unknown mechanism Akt inhibitor CD86, but not CD80, somehow enhances the store-independent activation of the CRAC channel,21,53 most likely in a STIM2/ORAI1 and/or ORAI3-dependent manner (Fig. 9b). In this model, the negative effect of CTLA-4 on T-cell activation is caused by the inhibition of CD28 recruitment to the IS. The knowledge of the fine-tuned difference in T-cell activation mediated by costimulatory molecules is of utmost importance not only to understand the underlying biology, but may also lead to novel therapeutic strategies that aim to activate the immune system against infectious

and malignant diseases. Super-agonistic antibodies targeting costimulatory molecules and activating T cells

by bypassing mTOR inhibitor the first signal have been developed in recent years.58 These super-agonistic antibodies bind to receptor domains that are not physiologically recognized by naturally occurring ligands, else circumvent the need for TCR specificity and, most importantly, are no longer regulated by the human immune system. This last issue has recently gained significant attention because a clinical trial using a CD28 super-agonistic antibody (TGN1412) confirmed in a dramatic manner that no model systems exists today that can predict immune mechanisms induced by super-agonistic molecules.58 In an early clinical trial performed in healthy volunteers, it was expected that activation of regulatory T cells by TGN1412 would further suppress the immune system and that the antibody would, eventually, be developed to treat patients with autoimmune diseases. As the CD28 antigen is expressed on the vast majority of T cells and not only on the small proportion of regulatory T cells, a broad T-cell activation pattern was observed resulting in a life-threatening cytokine release syndrome requiring treatement in the intensive-care unit. This clinical experience has demonstrated that the nature of super-agonistic, non-physiological ligands is unpredictable when tested in vivo. Along that line, a CTLA4–immunoglobulin has been developed for blockage of the CD28-CD80/CD86 pathway.

[18, 21, 23, 25, 28]

[18, 21, 23, 25, 28]

Mitomycin C concentration One study reported on the efficacy of amphotericin B in CPA with response rate of 82% whereas another study looked at a combination of itraconazole and micafungin and observed a response rate of 59%.[2, 28] A RCT has also compared micafungin with voriconazole, and found no difference in the efficacy between the two agents.[23] There is no randomised controlled study comparing antifungal agents with standard supportive therapy as done in our study. Subacute IPA: complete response – resolution of all signs and symptoms, nearly

complete resolution of radiological findings and other supportive evidence (mycology). Partial response – clinically meaningful improvement and >50% improvement in radiological findings. Stable disease – no or minor improvement in signs and symptoms and <50% radiological improvement. Failure – worsening of clinical and/or radiographic abnormalities CCPA: clinical, radiological and mycological CNPA: complete and partial responses Selleckchem HM781-36B CCPA: marked improvement in patient’s symptoms and signs, stable or improved radiology, and negative fungal cultures Response: clinical and/or radiological deterioration was absent Overall improvement: clinical improvement in the presence of radiographic stability, radiographic improvement in the presence of clinical stability, or combined clinical and radiographic improvement Success: improvement in at least two of the four groups of factors without deterioration in other two groups Failure: absence of success CNPA: 10/19 (53%) CCPA: 3/22 (14%)

Clinical crotamiton symptoms: improved (major symptoms and signs improved); unchanged; worsened Radiological (chest CT): area (cm2) was defined as maximum diameter multiplied by minimum diameter. Improvement (>50% reduction); Worsening (>25% growth); Unchanged (all other cases) Mycological and serological tests: clearance (documented clearance of infected sites plus normalisation of serological tests); presumed clearance (clearance of infected sites not documented and improvement in serological findings); persistent (documented Aspergillus spp. at infected sites or worsening in serological findings).

Previously, our group verified higher activity of mannose recepto

Previously, our group verified higher activity of mannose receptors on SB203580 mw macrophages from mice

pretreated with Con-A for 3 days compared to control group (Geraldino et al., 2010). In that study, Con-A-activated cells were able to destroy 70% of the C. albicans CR15 inoculum during 1 h of coincubation; however, macrophages from the control group killed only 30% of the pathogen. In this study, a reduction of 50.1 ± 3.6% in Candida phagocytosis was observed in the presence of mannan (100 μg mL−1) and 40.2 ± 3.8% in the presence of laminarin (100 μg mL−1), revealing higher activity of mannose and dectin-1 receptors on Con-A-activated macrophages, but not in PBS-macrophages (Table 1). Owing to the increase in the activity of mannose and dectin-1 receptors,

in this study, it was proposed that these pathways of phagocytosis could be mediating an adaptative immune response involving TH17 cells over the course of mouse infection with Candida. In the Con-A group, a significant increase in IL-17 concentrations occurred at 6 h postinfection that was maintained up to 18 h (Fig. 1). In the control group, analysis verified that the levels of IL-17 were significantly reduced over the course of infection compared to mice pretreated with Con-A (Fig. 1). Therefore, this study demonstrated the possibility that mannose and dectin-1 receptors could signalize R788 research buy the differentiation of TH17 cells with IL-17 production in the course of Candida infection in mice pretreated with Con-A. Corroborating these results, Van de Veerdonk et al. (2009) and LeibundGut-Landmann et al. (2007), reported that mannose receptors on human macrophages and dectin-1-activated dendritic cells from mice participate in the differentiation of naïve TCD4+ in effector T cells (TH-17 cells) in vitro in response to C. albicans. Although numerous studies have focused on the pathological aspects of IL-17-producing cells in autoimmune diseases, their role in protective antifungal immunity has also been increasingly Tyrosine-protein kinase BLK recognized (Conti & Gaffen, 2010;

Rehaume et al., 2010). Thus, our interest was to investigate whether the cytokines TGF-β, IL-1β and IL-6 could be driving the development of TH17 cells. Figure 2a shows basal levels of TGF-β in both groups; however, the levels of this cytokine were significantly higher in mice pretreated with Con-A 2 h postinfection, suggesting a trigger for TH17 differentiation. Corroborating these results, Mangan et al. (2006) demonstrated that TGF-β acted to promote a substantial increase in TH17+ cells independent of IL-23 in an experimental model under IFN-γ-null conditions; furthermore, the development of TH17 cells was impaired in TGF-β1-deficient mice, and also, IL-17 secretion was impaired in a dose-dependent manner when neutralizing antibody to TGF-β or IL-6 were present (Torchinsky et al., 2009). IL-6 production is dependent on signaling by dectin-1 receptor according to LeibundGut-Landmann et al.