Graft and patient survival were analysed using the Kaplan–Meier method. Pretransplant CMV D/R serostatus was available for the whole cohort, with EBV D/R serostatus available for 2566 transplants (56.8%).

Serostatus for both viruses was significantly associated with donor and recipient age and recipient smoking status. For both viruses the majority of transplants were in a D+/R+ serostatus setting: 45.3% for CMV and 77.9% for EBV. D/R serostatus for either virus did not have a significant effect on graft or patient survival. We conclude that in the current era of viral prophylaxis and surveillance, long-term outcome for the kidney transplant population is unaffected by D/R CMV and EBV serostatus. “
“A higher prevalence of sleep

apnoea (SA) has been observed in the chronic kidney disease (CKD) population compared with estimates in the general population. Increased rates of SA have been selleck compound described in patients with click here various renal-related diagnoses including dialysis, renal transplant, early-stage CKD and proteinuria. The mechanism or underlying aetiology for this association is different for each type of kidney disease. The extracellular fluid volume and metabolic derangements that characterize the uremic state likely contributes to SA in the dialysis population. SA causing direct renal insults from haemodynamic changes, ischaemic stress, or an intermediary condition such as hypertension, can lead to early CKD and proteinuria. While renal transplantation has cured SA in some patients, the post-transplant state is itself a risk factor for SA.

The high prevalence of SA in kidney disease and the associated clinical implications warrant vigilance in diagnosis and treatment of SA in the CKD patient. This review focuses on the prevalence of SA in patients with CKD including dialysis and transplant patients, and those with early-stage CKD and proteinuria. SA may vary in form and aetiology depending on type or stage of CKD. Based on these associations, we discuss our rationale for recommendations on screening and management of SA specific to the CKD population. The relationship between sleep apnoea (SA) and kidney disease represents a complex interaction of two disease processes where hypertension may or may not be an intermediary variable (Fig. 1). SA Verteporfin has been associated with several types of renal disease, including proteinuria, early- and late-stage chronic kidney disease (CKD), end-stage renal disease (ESRD) on dialysis and renal transplantation. It is unknown whether there is a causative association in either direction between CKD and SA, or whether the two diseases represent clinical sequelae from a more common disease process, such as diabetes mellitus, hypertension or neuropathy. Given the complexity and variety of renal disease associated with SA, there may be different grounds for each particular association.

However, the titers of 15L were clearly higher than those of 19L in two pairs (bottom two viruses), in contrast to previous reports (24, 26). If the loxP insertion at 143 nt or at 191 nt induces some difference to the viral packaging efficiency, a competition analysis would likely provide useful information. We performed a competition analysis using the 15L, 19L or ΔL virus together with a co-infected competitor virus, AxCAGFP (an AdV carrying a GFP-expression unit). The titers of these four AdV were approximately the same within the measurement error (Table 1), and the amounts of these viruses used to

infect the 293 cells were accurately readjusted for this analysis. The 15L, 19L or ΔL virus were each co-infected with the competitor virus at starting ratios of 1:0 (15L, 19L or ΔL only), 1:0.3, 1:0.03 and 0:1 (competitor only) MI-503 research buy (Fig. 2a). Serial passages using Tigecycline price 293 cells were performed, and DNA from each viral stock of the virus mixture was extracted, followed by XhoI digestion (Fig. 2b). The total DNA amounts of the mixed viruses were adjusted using the intensity of the band commonly derived from all virus genomes (shown as “common”, 2.5 kb). Because the genome flanked with loxP is not excised in 293 cells where Cre is not supplied, the bands derived from

15L, 19L and ΔL were almost identical in size because of the positional difference in the XhoI site, as shown in Figure 1 (4.0 kb, 3.9 kb and 4.1 kb, respectively). For each first stock, the intensities of the bands derived from 15L, 19L and the loxP-less ΔL containing the structure of the wild-type virus were similar (Fig. 2b, lanes 1, 5 and 9; the lane numbers are shown at the bottoms of the lanes), showing that the copy numbers of the viral genomes

were mostly identical after one cycle of viral replication in the 293 cells. Furthermore, in all three lanes, the bands for the 15L, 19L or ΔL were much thicker than that of the competitor virus Phosphoglycerate kinase (5.6 kb). However, these ratios of 15L and 19L changed drastically: the ratio was reversed in the third stock (lanes 2 and 5) and almost disappeared in the fifth stock, while the competitor virus increased (compare lane 3 with lane 1 and lane 7 with lane 5). Meanwhile, when ΔL was used, no significant changes occurred (compare lane 11 with lane 9). In the virus DNA patterns of the seventh stocks, the bands for 15L and 19L vanished and only the band for the competitor virus was detected (lanes 4 and 8), while the bands for ΔL were maintained (lane 12). Densitometry analysis quantitatively confirmed these observations (the percentages of the 15L, 19L or ΔL in the total virus DNA including the competitor were shown above the lane numbers). Moreover, these results were reproduced using an initial ratio of competitor virus of 1:0.03 (data not shown).

Given the postulated association of impaired neutrophil function as Dasatinib molecular weight a risk factor for melioidosis, G-CSF would be attractive as an adjunctive treatment

to improve outcomes of severe melioidosis with septicaemia. Studies have shown varying results regarding its use in the setting of severe sepsis. In a retrospective study from Australia comprising of 42 patients with septic shock and culture-confirmed melioidosis, mortality rates were significantly lower with G-CSF (10% vs 95% in historical controls without G-CSF therapy).[52] However, in a different setting with limited resources of intensive care from Thailand, in a randomized controlled trial comprising of 60 patients with severe sepsis suspected to be related to melioidosis, G-CSF was associated with a longer duration of survival (34 vs

15 h) but without any mortality benefit.[53] It is considered that the benefits of state-of-the-art intensive care facilities are far more important than a potential benefit of therapy with G-CSF.[12] Nevertheless, G-CSF is still used in the intensive care unit at Royal Darwin Hospital in patients with life-threatening melioidosis septic shock. Patients living in, or visiting from melioidosis endemic regions, see more or those with evidence of past exposure to B. pseudomallei (an indirect haemagglutination titre of >1:40), that are anticipated to commence immunosuppressive therapy, such as those enlisted for an organ transplant, should be screened for melioidosis. This entails a chest X-ray and microbial cultures of rectal and throat swabs placed into selective Ashdown’s broth, urine microscopy and culture, sputum culture if respiratory symptoms are present and culture on Ashdown’s agar of swabs from any skin lesions. Patients confirmed as culture positive should be treated for melioidosis as in Table 1. Patients who have no evidence of melioidosis can commence immunosuppression

and be active on transplant lists, but ongoing vigilance is essential for either activation of B. pseudomallei from a latent focus in those seropositive, or for new infection with B. pseudomallei in those continuing to live in an endemic acetylcholine location. In a recent systematic review by Peacock et al. it was concluded that from the studies to date in animal models, it should be theoretically possible to develop a vaccine for public-health purposes that would be cost-effective for the prevention of naturally acquired melioidosis in high-risk populations in hyper-endemic regions such as Thailand and tropical northern Australia.[54] However, at present there is no vaccine available for effective prevention of melioidosis, making general preventive measures and possibly anti-microbial prophylaxis the only available options for prevention currently.

After 48 h, cultures were pulsed with 0.4 μCi [3H]thymidine (Amersham Biosciences, Braunschweig, Germany),

and incubated for another 24 h. After harvesting, incorporated DNA was measured in a β-counter (Perkin Elmer, Rodgau, Germany). Cytotoxicity of freshly sorted splenic CXCR3− and CXCR3+ NK cells Ku-0059436 in vitro (5×105/mL) against YAC-1 target cells was assessed by standard 4 h chromium release assay. Target cells were labeled with 3 MBq Na51CrO4 (Hartmann Analytic, Braunschweig, Germany), incubated for 1 h at 37°C, washed two times and used for the assay within 1 h. Cells were plated in V-bottom 96-well plates. Background values were determined by incubating target cells without effector cells. Maximal values were obtained by lysing target cells with 1% Triton X-100 (Sigma-Aldrich).

After 4 h, cells were pelleted and 100 μL supernatant of each well was used for measurement of 51Cr release in a γ counter (MicroBeta/PerkinElmer, Waltham, MA, USA) in triplicates with E:T ratios of 10:1, 5:1, 2.5:1 and 1.25:1. Specific lysis was calculated by: [(experimental release–spontaneous release)/(maximum release–spontaneous release)] ×100. Lysosomal granule exocytosis was determined by CD107a expression. For this experiment, lymphocytes (E:T ratio 10:1) or sorted CXCR3− and CXCR3+ NK cells (E:T ratio 2:1) were incubated at 37°C in 5% CO2 together Selleck Staurosporine with YAC-1 cells for 4 h. Anti-CD107a mAb was added directly Adenosine triphosphate to the cell suspensions at a final concentration of 0.01 mg/mL. After 1 h of incubation, Monensin (BD Biosciences) was added as a golgi block at a final concentration of 5 μg/mL and incubation was continued for additional 3 h. In case of subsequent intracellular cytokine staining, brefeldin A (Sigma-Aldrich) was added at a final concentration of 2 μg/mL for the last 3 h of incubation time. Samples were finally surface-stained and analyzed via multicolor flow cytometry. In order to determine the IFN-γ production, sorted

CXCR3− and CXCR3+ NK cells were cultured in 96-well round-bottom culture plates (Greiner, Frickenhausen, Germany) in the presence of rIL-2 (100 U/mL), rIL-12 (10 ng/mL) and rIL-18 (5 ng/mL) for 15–17 h. Optimal cytokine concentrations were determined by earlier dose titrations. Brefeldin A (Sigma-Aldrich) was added at a final concentration of 2 μg/mL for the last 2 h of incubation time. Analysis of intracellular IFN-γ was preceded by surface staining at 4°C. After 30 min, cells were washed twice and resuspended in PBS containing 3% FCS. After fixation with 4% paraformaldehyde (Merck) for 10 min, cells were perforated with 0.1% saponin buffer (PBS supplemented with 0.1% saponin (Riedel-de Haën, Seelze, Germany) and 0.01 M HEPES (Roth, Karlsruhe, Germany)) and anti-IFN-γ mAb was added. After 30 min of incubation and three washes, cells were analyzed as described above.

05) to adhere to human alveolar (A549) and human

bronchial (BBM) epithelial cells. The XDR variant of KZN invaded A549 cells more effectively than the other isolates. These results suggest that the successful spread of the Beijing and KZN strains might be related to their interaction with alveolar epithelium selleckchem (Ashiru et al., 2010). Examples of the locally predominant, but drug-susceptible clonal groups emerge, intriguingly, from the insular settings. In Japan, a large-scale study of the Beijing genotype revealed that the spread of its modern Beijing sublineage, which has a high transmissibility, is currently increasing, while the spread of an ancient Beijing sublineage has decreased significantly in younger generations (Iwamoto et al., 2009). In another study in Trinidad island in Caribbean, it was shown that a single major clone of an ‘evolutionary modern’ tubercle bacilli (SIT566) was responsible for more than PF-02341066 ic50 half of the TB cases, whereas it preferentially infected younger age groups. A comparison with genotyping data for six Caribbean countries showed that the overall lineage distribution in Trinidad was completely different from its neighbors, i.e., Trinidad was the only country harboring a unique sublineage of the LAM family, designated

LAM-10CAM (Millet et al., 2009). This sublineage is phylogeographically specific for Cameroon and neighboring countries in West Africa; it was shown to be significantly associated with clusters, suggesting its preponderant role Osimertinib in recent transmission in Cameroon (Niobe-Eyangoh et al., 2004) and Burkina Faso (Godreuil et al., 2007). Interestingly,

3/4 of the patients within this group in Trinidad were African descendants (Millet et al., 2009). As mentioned above for the case of Beijing and KZN families in South Africa, the locally predominant clones may be noncompetitively cocirculating in an area. In Tunisia, >60% of the TB cases were due to a single genotype in each prevalent family, although their clustering differed: more clustered ST50/Haarlem was more predominant in the northern Tunisia, while the more widespread ST42/LAM displayed weak clustering and a low transmission rate, suggesting its stable association with the Tunisian population (Namouchi et al., 2008). Regarding interpretation of the results in our study, it should be noted, however, that ST125 was not associated either with drug resistance (Valcheva et al., 2008a) or with a higher growth rate in mouse macrophage model (N. Markova et al., unpublished data). The ability to replicate rapidly within macrophages may be considered as a proxy for increased transmissibility (Nicol & Wilkinson, 2008). Therefore, the presence of ST125 in Bulgaria cannot be attributed to the increased resistance/virulence/transmissibility properties. Instead, the specificity of ST125 in Bulgaria probably reflects its historical presence in this region, leading to a bacterium–host coadaptation.

Methods:  Visualization of arteriolar blood flow in rat cremaster muscle was carried out in both normal and reduced flow conditions before and after Dextran 500 infusion to simulate physiological and pathological levels of red blood cell aggregation

in humans. Results:  Both normalized mean (p < 0.0001) and SD (p < 0.002) of the layer width were significantly enhanced after hyper-aggregation induction in reduced flow conditions (mean pseudoshear rate = 57.3 ± 7.2/sec). Normalized mean and SD of the layer width generally increased with decreasing vessel radius and this effect was most pronounced with hyper-aggregation in reduced flow conditions. The threshold pseudoshear rate at which the layer formation became more pronounced when compared with non-aggregating condition was higher with hyper-aggregation (217/sec) than normal-aggregation induction (139/sec). Conclusion:  Our findings confirmed the formation Rucaparib solubility dmso of a prominent https://www.selleckchem.com/products/cx-5461.html cell-free layer in the arterioles under higher shear conditions at pathological aggregation levels and this effect became more pronounced in smaller arterioles in normalizing the layer to the vessel radius. “
“Microcirculation (2010) 17, 59–68. doi: 10.1111/j.1549-8719.2009.00009.x Purpose:  To quantitatively assess microvascular dimensions in the eyes of neonatal wild-type and

VEGF120-tg mice, using a novel combination of techniques which permit three-dimensional (3D) image reconstruction. Methods:  A novel combination of techniques was

developed for the accurate 3D imaging of the microvasculature and demonstrated on the hyaloid vasculature of the neonatal mouse eye. Vascular corrosion casting is used to create a stable replica of the vascular network and X-ray microcomputed tomography (μCT) to obtain the 3D images. In-house computer-aided image analysis techniques were then used to perform a quantitative morphological analysis of the images. Results:  With the use of these methods, differences in the numbers of vessel segments, their diameter, and volume of vessels in the vitreous compartment were quantitated in wild-type neonatal mice or littermates over-expressing a labile (nonheparin binding) isoform of vascular endothelial growth factor (VEGF120) from the developing lens. This methodology was instructive in demonstrating that hyaloid vascular networks in VEGFA120 over-expressing mice have why a 10-fold increase in blind-ended, a six-fold increase in connected vessel segments, in addition to a sixfold increase (0.0314 versus 0.0051 mm3) in total vitreous vessel volume compared with wild type. These parameters are not readily quantified via histological, ultrastructural, or stereological analysis. Conclusion:  The combination of techniques described here provides the first 3D quantitative characterization of vasculature in an organ system; i.e., the neonatal murine intra-ocular vasculature in both wild-type mice and a transgenic model of lens-specific over-expression of VEGF.

Similar events may be initiated in T cells by ICs and complement activation in autoimmune disorders. Syk has been a target for therapeutic intervention for autoimmune diseases. Syk-mediated signalling contributes to the altered T cell signalling [31]. In this report, we demonstrate that the FcγRIIIA/B receptor engagement by ICs on CD4+

T cells leads to the recruitment of the signalling subunit, the FcRγ chain, thus resulting in Syk activation. The BIBW2992 ic50 presence of soluble TCC enhances this signalling event. TCC in fluid phase by associating with vitronectin (S protein) becomes cytolytically inactive and is regarded as irrelevant. However, recent reports have shown that TCC induces functional activities such as kinin-dependent vascular leakage, activation of endothelial cells and induction of osteoprotegerin [16,32,33]. Vitronectin facilitates the cellular adhesion of soluble TCC, providing a mechanism to trigger cellular responses [34]. Previously, we have shown elevated levels of vitronectin associated with membrane attack complex (MAC) in lupus nephritis patients [23]. Our results point to a synergistic

role for TCC in IC-mediated Syk activation in CD4+ T cells. Such synergistic action of ICs and MAC in chemokine secretion during lung tissue injury has also been reported previously [35]. Binding of AHG (Fig. 1) and ICs purified from SLE Benzatropine to the peripheral CD4+ T cells establishes the interaction and a possible role of ICs in T cell responses. Previously, activation-dependent selleck chemical expression of FcγRII and FcγRIII receptors in the human T lymphocyte subpopulation has been observed [36]. This study showed a four- to 10-fold increase in the FcγRIII+ CD8+ T cell population in response to phytohaemagglutinin (PHA) treatment on day 3 post-stimulation [36]. Our results also point to a similar phenomenon, where FcγRIII+CD4+

T cells expanded in vitro using anti-CD3 and CD28, a total of more than 40% cells stained for FcγRIIIA/B in comparison to 10% directly from the PBMC. To explore whether ICs can influence the T cell physiology, we investigated the role of these complexes in Syk activation. Syk is a homologue of non-receptor tyrosine kinase ZAP-70. Syk is activated by FcRγ chain upon ITAM phosphorylation. Syk is expressed widely in both immune and non-immune cells [37,38]. Both DAP-12 and FcγR associate with Syk and mediate β-2 integrin signalling in neutrophils and macrophages [39]. Syk phosphorylation also occurs upon engagement of pathogen recognition receptors such as FcγR, CR3 and Dectin-1 [1]. Accumulating evidence points to Syk expression in subsets of T lymphocytes such as thymocytes, naive αβ T cells and intraepithelial γδ T cells, but not in proliferating and mature T cells [31,40].

, 2007). The biofilm serves as a skeleton for large numbers of bacteria within a single structure and confers the population of interacting organisms with protection, one of the hallmarks of multicellular organisms. Extending the skeletal

metaphor, the biofilm matrix also plays important roles in signaling control and nutrient availability. Rheological studies by Stoodley and colleagues have demonstrated that the hydrated EPS matrix is highly viscoelastic and can be rapidly remodeled ABT 263 in response to changes in shear and other environmental stressors (Dunsmore et al., 2002; Klapper et al., 2002; Stoodley et al., 2002; Towler et al., 2003; Shaw et al., 2004). Thus, in this regard, it displays qualities similar to endochondral bone in that the strength of the extracellular matrix is modifiable by the cellular component in accordance with the external load. Detailed imaging and metabolic studies spurred by the development of the confocal microscope and PCR-based diagnostics have revealed that many disease conditions that were previously thought of as being chronic inflammatory in nature are actually indolent bacterial biofilm infections. These include osteomyelitis associated with S. aureus and Staphylococcus

epidermidis (Marrie & Costerton 1985; Costerton, 2005); gall bladder disease (Sung et al., 1991; Stewart et al., 2007); various chronic middle-ear disease processes associated with H. influenzae, S. pneumoniae, LDK378 purchase Moraxella catarrhalis, and Pseudomonas aeruginosa including otitis media with effusion, recurrent otitis media, and otorrhea (Rayner et al., 1998; Ehrlich et al., 2002; Post et al., 2004; Dohar et al., 2005; Hall-Stoodley et al., 2006; Bakaletz, 2007; Kerschner et al., 2007; Post & Ehrlich, 2007, 2009; Apicella, 2009); chronic rhinosinusitis associated with H. influenzae, S. aureus, and other bacteria (Palmer, 2006; Sanderson Protein kinase N1 et al., 2006; Psaltis et al., 2007; Prince et al.,

2008); cholesteatoma associated with P. aeruginosa (Chole & Faddis, 2002); tonsillitis (Chole & Faddis, 2003); and adenoiditis associated with H. influenzae, S. pneumoniae, and M. catarrhalis (Zuliani et al., 2006; Nistico et al., 2009). In addition, there is substantial evidence to support a bacterial biofilm etiology for many chronic infections of the urogenital systems of both men and women including cystitis, prostatitis, vaginitis, and endometritis (Nickel et al., 1994; Hua et al., 2005; Swidsinski et al., 2008), and recently, both S. aureus and S. epidermidis have been demonstrated to form biofilms at surgical site infections (Kathju et al., 2009). Biofilms are also associated with dental infections including plaque, endodontitis (Carr et al.

The three baseline factors independently associated with renal atrophy (identified by the univariate Cox proportional analysis) were systolic hypertension, severity of RAS and diminished renal cortical blood flow velocity. A 1.9-fold and 1.6-fold

increase in selleck kinase inhibitor the risk of renal atrophy was associated with every 20 mmHg increase in systolic BP and 10 mmHg increase in diastolic BP, respectively, at the follow-up examinations. The use of ACE inhibitors at baseline showed no significant association with renal atrophy even in kidneys with significant stenosis. There was no significant association between the presence of accessory renal arteries and a decreased risk of atrophy. Finally, the mean change in serum creatinine concentration was +7 µmol/L per year and +29 µmol/L per year in participants with atrophy detected in one kidney and both kidneys, respectively. In an observational series of patients with ARVD using intravenous pyelography, Dean et al. demonstrated a stability (<5% reduction) in renal sizes in 37% of patients,

mild to moderate decrease (5–9%) in 26% of patients and significant (>10%) reduction in kidney length (equated to 30% decrease in renal mass) in 37% of patients.10 This study supports the hypothesis that ARVD could be associated with progressive renal atrophy. However, there was little data relating renal atrophy to degree of baseline stenosis. The study by Schreiber et al. used angiographic images for kidney sizes and reported a reduction in renal size in 70% of patients see more with progressive ARVD compared with 13% in those with stable stenosis (P < 0.001). However,

there is little information about the side of the stenosis, the side of renal atrophy and correlation between them.9 A number only of longitudinal studies have demonstrated a decline in kidney function over time in patients with ARVD. Schreiber et al. reported change in serum creatinine in different categories of baseline stenosis (<50%, 50–75%, 75–99% and 100%) over a mean follow-up period of 52 months. An increase in serum creatinine levels was seen in 54% of patients with progressive disease (defined as change from one category of stenosis to a category of higher grade stenosis), while an increase was observed in only 25% of patients without evidence of angiographic progression.9 However, these data are limited by the use of serum creatinine, which is a poor indicator of individual kidney function as a marker of renal function. Chabova et al. in a retrospective cohort study at the Mayo Clinic, looked at 68 patients with angiographically proven high-grade stenosis (>70%) over a mean period of 38.9 months. Serum creatinine rose from 124 µmol/L to 176 µmol/L for the entire group. This result was skewed by 10 patients (14.7%), 6 of whom developed end-stage kidney disease.

We acknowledge the Wellcome Trust, NIHR Biomedical Research Centre Programme

(Oxford) and the MRC. None. “
“Inflammatory DCM (iDCM) may be related to autoimmune processes. An immunoadsorption (IA) has been reported to improve cardiac hemodynamics. The benefit of IA is probably related to the removal of autoantibodies. A recent study suggests additional effects of IA on the T cell–mediated immune reactions, especially on regulatory T cells (Tregs). In this prospective study, the correlation between the level of Tregs and improvement of myocardial contractility in response to IA in patients with iDCM was investigated. Patients (n = 18) with iDCM, reduced left ventricular (LV) ejection fraction (<35%), were enrolled for IA. Before and 6 months Selumetinib chemical structure after IA, LV systolic function was assessed by echocardiography, and blood levels of Tregs were quantified by FACS analysis. Patients (n = 12) with chronic ischaemic heart failure and comparable reduced LV-EF served as controls. IA improved CHIR-99021 price LV-EF in 12 of 18 patients at 6-month follow-up. These patients were classified as ‘IA responder’. In 6 patients, LV-EF remained unchanged. At baseline, IA responder and non-responder subgroups showed similar values for C-reactive protein,

white blood cells, lymphocytes and T helper cells, but they differ for the number of circulating Tregs (responder: 2.32 ± 1.38% versus non-responder: 4.86 ± 0.28%; P < 0.01). Tregs increased significantly in the IA responders, but remained unchanged in the IA non-responders. In patients with ischaemic

cardiomyopathy, none of these values changed over Dimethyl sulfoxide time. A low level of Tregs in patients with chronic iDCM may characterize a subset of patients who do best respond to IA therapy. Dilated cardiomyopathy (DCM) is defined by an impairment of myocardial contractile function and ventricular dilation. In a subset of patients, the etiopathophysiology of DCM is linked to autoimmune reactions, characterized by the appearance of cardiotoxic autoantibodies in the blood and signs of myocardial inflammation. In about 2/3 of patients with autoantibodies, viral or bacterial RNA or DNA can be detected in myocardial biopsies, suggesting that these immunological features are initiated by an infectious process [1-3]. A (non-ischaemic) DCM with an autoimmune- or immune-mediated infectious background has been termed as inflammatory DCM (iDCM). A variety of autoantibodies against cardiac cell proteins have been identified in patients with iDCM [3]. Of note, many of these autoantibodies (e.g. targeting ß1-adrenergic receptor, muscarinic M2-acetylcholine receptor, myosin, Na-K-ATPase, troponin I) belong to the IgG subclass 3 that has the highest antibody-dependent potency for cellular toxicity [4]. Wallukat et al.