By immunohistochemical staining, we confirmed Thy-1 expression on ECs derived from OVA-immunized WT mice (Fig. 4B) and a lack of Thy-1 expression on ECs in Thy-1−/− mice (Fig. 4D). Most importantly, Thy-1 was also not detectable on ECs in the lungs of chimeric mice, but several cells in the inflammatory infiltrate (most likely TCs) were Thy-1 positive check details (Fig. 4F). To exclude any effects of the lack of Thy-1 on TCs on the control of the extravasation of eosinophils during acute inflammation, chimeric mice were immunized with OVA, according to the standard protocol. Thy-1−/− mice and WT mice were immunized as controls. As shown in Fig. 5A, the total number of inflammatory cells in the BAL

was significantly diminished in Thy-1−/− mice as well as in chimera, Autophagy Compound Library price compared to WT mice. Differential staining showed that the number of both eosinophils and macrophages in the BAL fluid was diminished

in Thy-1−/− mice as well as in chimera, compared to WT mice (Fig. 5B). Thus, although Thy-1−/− BM chimera expressed Thy-1 on 70% of TCs and Thy-1−/− mice did not express Thy-1 on TCs, in both mice the extravasation of leukocytes, especially eosinophils, was significantly reduced, compared to the WT mice. These results confirm that the decreased infiltration of the lung in Thy-1−/− mice was not merely a consequence of the lack of Thy-1 expression on TCs. We have shown that Thy-1 is involved in the control Prostatic acid phosphatase of leukocyte recruitment during inflammation. Next, we ask whether Thy-1-dependent leukocyte extravasation during inflammation has further functional

consequences, such as the release of chemokines, cytokines, and proteases by the leukocytes. To address this issue, BAL and peritoneal fluid of WT and Thy-1−/− mice were compared. Cytokine and chemokine expression in the BAL was analysed by a membrane-based cytokine/chemokine array. The array results represent the chemokine/cytokine profile of three different WT and Thy-1−/− mice, respectively (Fig. 6). In the BAL of WT mice IL-4, IL-5, eotaxin-2 (CCL24), TARC (CCL17), and MIP-1α (CCL3) were augmented (quotient >1.25), compared to Thy-1−/− mice (Fig. 6A). Analysis of mRNA expression of CCL3, CCL17, CCL24, IL-4, and IL-5 by semi-quantitative PCR revealed that these mediators were expressed by eosinophils and monocytes (Fig. 6B). In peritoneal fluid of WT mice, eotaxin-2 was also enhanced twofold, compared to Thy-1−/− mice (data not shown). In addition, we quantified the amount of MMP-9 since it is an important protease for the degradation of basement membrane components and, thus, plays a critical role during the transmigration of cells through basement membranes. MMP-9 was analysed by ELISA in the BAL and peritoneal fluid of WT mice and Thy-1−/−mice. Induction of lung inflammation by OVA challenges upregulated MMP-9 in BAL (Fig. 6C). Indeed, a significant decrease of MMP-9 levels was seen in the BAL of Thy-1−/− mice, compared to WT mice (Fig. 6C).

) Their BM aspiration was performed as a part of routine diagnostic evaluation. Subsequently, their BM found to be normal haematologically. Flowcytometry based phenotyping using specific antibodies against CD3 (PE; BD Pharmingen, San Diego,

CA, USA), CD161 (Cy5PE; BD Pharmingen) and Vα24 (FITC, Dako Coulter, Glostrup, Denmark)/Vβ11 (FITC; Serotec, Kidlington, UK)/iNKT (FITC; BD Pharmingen) showed an increase in the frequency of iNKT (CD3+ CD161+ Vα24/Vβ11+) cells GSK126 order in blood (n = 28; percent mean ± SD, 1·35 ± 1·66) of freshly diagnosed patients compared with that of healthy controls (n = 17; percent mean ± SD, 0·34 ± 0·24) (Figure 1a,b,e). iNKT cells are also enriched in the BM of patients with VL (n = 17; percent mean ± SD, 1·19 ± 1·17) as compared with NBM (n = 9; percent mean ± S.D., 0·34 ± 0·13) (Figure 1c,d,f). The enrichment of iNKT cells was disease specific, as their frequency is significantly buy APO866 decreased after successful therapy (post-therapy) (Figure 1e,f). To observe the frequency of CD1d reactive cells, we mixed αGalcer with CD1d dimer (in 40× molar excess ratio). The mononuclear cells derived from blood and BM were stained with αGalcer-loaded CD1d dimer (Supporting information Figure S1). Frequency of αGalcer-loaded CD1d-reactive

NKT cells remains unaltered in blood and BM, as compared with blood of HCs (Figure 1g,h). In our effort to enumerate the parasite-specific CD1d reactive cells, we loaded CD1d dimer

with LPG (Supporting information Figure S2). The frequency of LPG-loaded CD1d+ NKT cells derived from BM ranges from 0·2 to 0·7% in a limited number of patients (n = 5) BIBF1120 (Figure 1i). In context to human VL, it would also be interesting to observe the response of iNKT cells against various lipid antigens of L. donovani, particularly LPG and GPIL. Reports suggest that L. donovani-infected kupffer cell activates iNKT cells (10) and activation of iNKT by αGalcer augments the disease pathology among L. donovani-infected mice (11). Our preliminary finding in a limited number of patients (n = 4) suggests that iNKT cells produce both IFN-γ as well as IL-4 in response to polyclonal stimulation (Supporting information Figure S3). To add further, αGalcer stimulates the production of IFN-γ and IL-4 by iNKT cells (6). Developing an analogue of αGalcer, which selectively produce either IFN-γ or IL-4, will be appropriate in tuning the right kind of iNKT cells. Recent development in human-specific thioglycoside analogue of αGalcer, which triggers the production of IL-12 and IL-10 by iNKT cells (12), suggests it as a candidate vaccine of immense potential. Identification of a pro-inflammatory IL-17 producing subset of iNKT cells inflates its potential under diseased condition (13). Triggering iNKT cells and thus modulating immune response among patients with VL might result in favour of host depending on their capacity to produce IFN-γ and IL-17.

Although the relation of elicited play to verbal IQ and its constituent subtests fell short of statistical significance, elicited play predicted poorer verbal working memory on the Digit Span test, confirming that this measure of the development of symbolic play competence in infancy may provide find more an early indicator of verbal working memory ability or early

executive function. The relation of symbolic play in infancy to FASD diagnosis at 5 years was examined using analysis of variance (Table 7). Whereas spontaneous play was unrelated to diagnosis, mean elicited play levels were lower for infants subsequently diagnosed with FAS/PFAS and also for the nonsyndromal heavily exposed infants when contrasted

to the abstainers/light drinkers. Post hoc tests showed that elicited play scores see more were lower for both the FAS/PFAS (p < .01) and other heavy exposed (p < .025) infants compared with abstainers/light drinkers. This study confirms the association between fetal alcohol exposure and elicited play in this heavily exposed Cape-Colored population that was first reported in a moderately exposed, inner city African American cohort in Detroit. In both the Cape Town and Detroit cohorts, the observed relation of prenatal alcohol exposure to spontaneous play was attributable to being reared in a less optimal social environment. In contrast, in both cohorts the association with elicited play remained significant after controlling for these influences, Y-27632 price indicating an impact of prenatal alcohol that is independent of the adverse effects associated with being raised

in a less optimal social environment. The effect of prenatal alcohol exposure on elicited play suggests that this exposure is associated with a delay in the development of competence as the infant proceeds through the stages of mastering symbolic play. Alternatively, prenatal alcohol exposure may interfere specifically with the child’s ability to model his/her behavior to that demonstrated by the examiner, a capacity that plays an important role throughout early cognitive development. The replication of these findings in a sample of children whose ethnic and sociocultural background differs markedly from the original Detroit cohort and the distinct effects of alcohol exposure and environment on these two forms of symbolic play attest to the robustness of these effects. These data also demonstrate that the social environment plays a critical role in the rate at which the infant progresses through the stages of both performance and underlying competence in mastering symbolic play, as indicated by both the spontaneous and elicited play measures. Bradley et al. (1989) distinguish between process and status environmental factors in relation to mental development.

23 Rainer et al. [14] developed a selective SceSel+ medium containing dichloran and benomyl as active compounds, which inhibits a large diversity of filamentous

fungi. The SceSel+ medium prevented growth of Aspergillus in sputum samples; Scedosporium strains are overgrown or outcompeted on full medium by Aspergillus strains, due to faster growth rates of A. fumigatus strains. Blyth et al. [13] shows that benomyl-media are significantly more efficient for selective isolation of Scedosporium species than for routine media such as SGA, with up to 100% Syk inhibitor recovery of Scedosporium from spiked samples when SceSel+ was used. When sputum samples are processed with benomyl-based media, recovery rates

tend to increase significantly: Horréet al. [24] noted 14.3% positive samples and Blyth et al. [13] 14.7%. Although our isolation procedure included the use of DRBC-benomyl agar, our isolation rate (8.5% positive) was somewhat in the lower range. When experimental non-culture methods are used to detect Scedosporium in CF sputum samples, significantly higher recovery rates are obtained. Cimon et al. [15], using counterimmuno-electrophoresis were able to raise the detection rate to 21.1% positive samples, compared to 8.6% with classical selleck chemicals culture. In the present study, we found 62.7% of the samples positive by PCR-RLB. The phenomenon that PCR-based diagnostic Atazanavir assays detect substantially more positives is an often-encountered problem.

A disadvantage of PCR is the risk of false-positive results, caused by either pre-PCR contamination of samples, non-specific amplification or by amplification of DNA from dead cells. Careful precautions against cross-contamination were taken during sample collection and preparation by using separated rooms and filtered tips. No cross reaction or false positive in tester strains was found. All clinical samples were processed twice and identical results were obtained. Therefore, the chance of false-positivity due to contamination or non-specific amplification is negligible. In 10 samples two or three species were detected. These results suggest the regular inhalation of fungal spores belonging to different species of the P. apiosperma/P. boydii complex and the subsequent colonisation of the respiratory tract or at least their persistence in the airways.10 The prevalence of Scedosporium DNA in the environment and the air presently is unknown, which hampers to ascertain whether or not real colonisation has taken place in patients with positive samples. To clarify this, further study is necessary. In one case, PCR-RLB was negative although the sample was proven to be positive by culture. The single deviating Scedosporium culture-positive sample was repeatedly negative using PCR-RLB and remained so with a 1 : 5 dilution of the DNA extract.

At least 100 cells were differentiated by light microscopy based on conventional morphologic criteria. Neutrophils displayed a multilobed nucleus and a fine pink staining. Eosinophils are characterized by the bilobed nucleus and deep pink staining of the cytoplasm. Lymphocytes have got a large, round, deeply blue nucleus. Monocytes were identified by the kidney shaped or bilobed nucleus. Cell-free BAL supernatant was collected for cytokine and MMP-9 Epacadostat research buy detection. Mice were injected i.p. with 1 mL of 3% thioglycollate media (BD Biosciences) or PBS as control. At indicated time points peritoneal lavage was collected. Cells in the lavage fluid were counted and

cell differentials were determined on slide preparations stained with Diff Quik (Dade Behring, Marburg, Germany). Cells were differentiated as described above. Cell-free peritoneal fluid was collected. Peritoneal tissue was dissected for histological studies. We greatly appreciate the Z-VAD-FMK nmr technical assistance of Mr. Danny Gutknecht. We thank Manuela Ackermann for performing i.v. injection and Jutta Jahns for irradiation of mice. This work was

supported by the Deutsche Forschungsgemeinschaft to Anja Saalbach and Ulf Anderegg (SA 683/2-1). Conflict on interest: The authors declare no financial or commercial conflict of interest. Detailed facts of importance to specialist readers are published as ”Supporting Information”. Such documents are peer-reviewed, but not copy-edited or typeset. They are made available as submitted by the authors.

“
“Successful embryo implantation occurs followed by a local inflammatory/T helper type 1 (Th1) response, subsequently redirected towards a tolerogenic predominant profile. The lack of control of this initial local inflammatory response may be an underlying cause of early pregnancy complications as recurrent spontaneous abortions (RSA). Considering that Thiamine-diphosphate kinase vasoactive intestinal peptide (VIP) mediates anti-inflammatory and tolerogenic effects in several conditions we hypothesized that VIP might contribute to tolerance towards trophoblast antigens during the early interaction of maternal leucocytes and trophoblast cells. In this study we investigated VIP/VPAC system activity and expression on maternal peripheral blood mononuclear cells (PBMCs) after interaction with immortalized trophoblast cells (Swan-71 cell line) as an in-vitro model of feto–maternal interaction, and we analysed whether it modulates maternal regulatory T cell (Treg)/Th1 responses. We also investigated the contribution of the endogenous VIP/VPAC system to RSA pathogenesis. VIP decreased T-bet expression significantly, reduced monocyte chemotactic protein-1 (MCP-1) and nitrite production in co-cultures of PBMCs from fertile women with trophoblast cells; while it increased the frequency of CD4+CD25+ forkhead box protein 3 (Foxp3)+ cells, transforming growth factor (TGF)-β expression and interleukin (IL)-10 secretion.

The tench were dissected and sexed before the digestive tract from each was removed and opened longitudinally in search of helminths. For tapeworms found still attached to the intestine, their position was registered before a 15 × 15 mm piece of tissue that surrounded the site of attachment was excised and then fixed in either chilled (4°C) bouins or in 10% neutral buffered formalin for 24 h. The bouin

fixed material was subsequently rinsed in several changes of 4°C 70% ethanol before being stored in the same medium until processed for histology. After fixation, the tissues were dehydrated through an alcohol series and then paraffin RG7204 nmr wax embedded using a Shandon Citadel 2000 Tissue Processor (Shandon Citadel 2000, London, UK). After blocking out, 5-μm-thick sections were cut and then stained with haematoxylin and eosin and/or alcian Doxorubicin order blue 8 GX pH 2·5 and periodic acid Schiff’s reagent (AB/PAS). Multiple histological sections were taken from each tissue block, examined and photographed using a Nikon Microscope ECLIPSE 80i (Nikon, Tokyo, Japan). For transmission electron microscopy (TEM), 7 × 7 mm pieces of infected intestinal tissue were fixed in chilled 2·5% glutaraldehyde in

0·1 m sodium cacodylate buffer for 3 h. The fixed tissues were then post-fixed in 1% osmium tetroxide for 2 h and then rinsed and stored in 0·1 m sodium

cacodylate buffer containing Amoxicillin 6% sucrose for 12 h. Thereafter, the pieces of tissue were dehydrated through a graded acetone series and embedded in epoxy resin (Durcupan ACM, Fluka). Semi-thin sections (1·5 μm) were cut on a Reichert Om U 2 ultra microtome and stained with toluidine blue. Ultra-thin sections (90 nm) were stained with 4% uranyl acetate solution in 50% ethanol and Reynold’s lead citrate and then examined using an Hitachi H-800 transmission electron microscope (Hitachi H-800, Tokyo, Japan). For each method, corresponding pieces of uninfected intestine were also processed, so that a direct comparison with the infected material could be made. For comparative purposes, the number of granulocytes in an area measuring 30 000 μm2 was determined using a Nikon Microscope ECLIPSE 80i and computerized image analysis software (Nis Elements AR 3.0) in 10 separate zones on each section of infected fish (i.e. in the submucosa layer close to the site of cestode attachment) and in 10 separate areas on each section of uninfected fish material. Granulocyte subsets (i.e. neutrophils and mast cells) were identified on subcellular features observed using transmission electron microscopy.

In agreement with this, reduced mitochondrial membrane potential was observed in motor neurones cultured from G93A mSOD1 mice, buy CH5424802 suggesting mitochondrial functional defects may have secondary effects on the dynamic status of mitochondria, impacting on their morphology [115]. Accumulation of proteins is a hallmark pathology of ALS and is an indicator of defective axonal transport (Figure 3). Accumulations of neurofilaments

and peripherin occur as either perikaryal aggregations [hyaline conglomerate inclusions (HCIs)] or axonal spheroid swellings. HCIs occur in SOD1-mediated FALS patients and consist of both phosphorylated and nonphosphorylated neurofilaments [117,118]. Accumulations of neurofilaments and decreased transport of cytoskeletal proteins were shown in the G93A, G85R and G37R SOD1 mice [119]. Importantly, these defects in slow axonal transport were observed at least 6 months prior to disease onset [119]. Mutations in dynein and the dynactin complex have also been implicated

in FALS, suggesting disruption to dynein-mediated fast axonal transport may be pathogenic. Mutations in the p150 subunit of dynactin have been identified in several FALS cases [120,121]. KIF5A mutations have also been found in patients with a related motor neurone disorder, hereditary spastic paraplegia [122]. Pathogenic mutations in KIF5A were shown to perturb KIF5A-mediated motility [123]. Axonal transport of mitochondria was disrupted filipin in a mouse model of mutant spastin-induced hereditary spastic paraplegia [124]. These lines of evidence indicate that Histone Methyltransferase inhibitor defective mitochondrial axonal transport is an early and important event not only in ALS, but also in other motor disorders, and may be a common pathway in different complex disorders. In motor neurones from G93A mSOD1 mice and primary cortical neurones transfected with four different SOD1 mutants,

anterograde transport of mitochondria was selectively impaired [115]. This was associated with decreased mitochondrial membrane potential and rounding up of mitochondria, indicative of mitochondrial dysfunction [115]. In addition, mSOD1 targeted to the mitochondrial IMS is sufficient to cause axonal transport defects of mitochondria [109]. Redistribution of damaged mitochondria might serve as an additional insult to motor neurones, particularly in the distal axon segment. This agrees with data from in vivo models and human ALS patients [108], where dying back of the distal axon is an early and potentially catastrophic event. Motor proteins and their associated adaptor proteins may be damaged by mSOD1, impairing axonal transport. Although there has been no direct interaction found between kinesin and mSOD1, the adaptor proteins Milton and Miro may be important in the regulation of axonal transport of mitochondria via mSOD1-induced changes to calcium levels.

Figure S1. Flow cytometric gates for the evaluation and collection of B lineage cells from the bone marrow of 8-week C57BL/6 mice. Table S1. CDR-H3 sequences obtained from wild-type C57BL/6 bone marrow B lineage cells Table S2. CDR-H3 sequences obtained from C57BL/6 IgHa.ΔD-iD congenic bone marrow mature, recirculating

B cells. “
“There is emerging interest in the application of mesenchymal stem cells (MSC) for the prevention and treatment of autoimmune diseases, graft-versus-host disease and allograft rejection. It is, however, unknown how inflammatory conditions affect phenotype and function of MSC. Adipose tissue-derived mesenchymal www.selleckchem.com/products/ABT-888.html stem cells (ASC) were cultured with alloactivated peripheral blood mononuclear cells (PBMC) (mixed lymphocyte reaction: MLR), with proinflammatory cytokines [interferon (IFN)-γ, tumour necrosis factor (TNF)-α and interleukin (IL)-6] or under control conditions,

and their full genome expression and function examined. Proinflammatory cytokines mainly increased indoleamine-2,3-dioxygenase expression, whereas ASC cultured with MLR showed increased expression of COX-2, involved in prostaglandin E2 production. Both conditions had a stimulatory, but differential, selleck chemicals effect on the expression of proinflammatory cytokines and chemokines, while the expression of fibrotic factors was decreased only in response to proinflammatory cytokines. Functional analysis demonstrated that inflammatory conditions affected morphology and proliferation of ASC, while their differentiation capacity and production of trophic factors was unaffected. The immunosuppressive capacity

of ASC was enhanced strongly under inflammatory conditions. In conclusion, ASC showed enhanced immunosuppressive capacity under inflammatory conditions, while their differentiation capacity was preserved. Therefore, Tenoxicam in vitro preconditioning provides ASC with improved properties for immediate clinical immune therapy. Mesenchymal stem cells (MSC) are found in a variety of tissues, including bone marrow, skin and adipose tissue [1–3] and can be expanded easily in vitro. MSC are thought to have tissue regenerative properties, in the first place via their multi-lineage differentiation capacity [2] and, perhaps more importantly, via the secretion of trophic factors that may activate local progenitor cells [4]. In addition, MSC have potent immunomodulatory capacity. They inhibit the proliferation of T cells [5,6] and inhibit dendritic cell maturation [7,8]. These properties make MSC promising for a diversity of clinical applications; for example, for the prevention and treatment of autoimmune diseases and bone marrow rejection. Recently, interest has developed in the use of MSC in solid organ transplantation [9,10]. These conditions are associated with an inflammatory milieu.

Therefore, we cell sorted pre/pro-B cells, immature BAFF-R positive and negative cells and mature B cells and reanalyzed them for BAFF-R expression (Fig. 6C) and IgM expression (Fig. 6D). As shown in Fig. 6D, BAFF-R expression correlated with up-regulated surface IgM levels; BAFF-R-positive

cells expressing high levels of BCR compared with BAFF-R-negative immature B cells. Moreover, like in mouse an inverse correlation between surface BAFF-R and RAG-2 expression, as an indication for active recombination, could be observed in human immature B cells (Fig. 6E). BAFF-R– immature B cells expressed 20–75% of the RAG-2 level found in selleckchem pre/pro-B cells, whereas BAFF-R+ immature B cells only expressed 3–20% of this level (Fig. 6E). As expected, no RAG-2 was detectable in mature B cells. The limited availability of human BM samples as well as the reduced number of cells recovered upon cell sorting hampered us to perform in vitro receptor editing experiments. Nevertheless, based on the correlation between surface IgM and relative quantification of RAG2 transcript, for human immature BM B cells, BAFF-R expression seems to be a marker for ‘bona fide’ positively selected cells also on human immature BM B cells. The generation of Staurosporine anti-mouse as well as anti-human BAFF-R monoclonal antibodies allowed us to carefully analyze the expression pattern of BAFF-R by B cells at various

developmental stages. Our analysis Adenosine triphosphate revealed that FACS-detectable BAFF-R expression was first observed on a subpopulation of immature BM B in both species. BM immature B cells represent the first stage of developing B cells at which a complete BCR is expressed at their surface. Moreover, they represent a critical stage for B-cell selection. Auto-reactive as well as non-functional B cells have to be deleted from the pool of immature B cells, whereas B cells bearing a functional BCR can develop further into mature B cells. While mechanisms underlying negative selection have been described, it remains to be understood how positive selection occurs. In this regard, a potential candidate

molecule capable of delivering the required survival signals to developing B cells could be the BAFF-R. The BAFF-R belongs to the TNF-R superfamily and was shown to signal via the alternative NF-κB pathway, delivering pro-survival signals to mature B cells. In terms of positive selection, the correlation between BAFF-R and BCR expression levels within BM immature B cells prompted us to hypothesize a functional axis between these two receptors. Thus, we hypothesize that the expression of a functional non-auto-reactive BCR at the immature B-cell stage induces surface BAFF-R. The BCR and BAFF-R in conjunction with PI3 kinase signaling 29–32 mediate the required activation threshold necessary to ensure survival of the developing B cell for the time necessary to achieve complete cell maturation.

Renal biopsy can be used to determine whether the patients are associated with idiopathic or secondary renal glomerular disease and identify the pathological type of glomerulopathy. However, the anatomical structure of HSK and complex relations to adjoining great vessels and organs increase the difficulty and risk of renipuncture,[5] which is the primary reason for why there are fewer HSK cases who receive renal biopsy. We believe that renal glomerular disease of HSK is one of the possible

factors leading to proteinuria, haematuria and renal dysfunction. Therefore, that the pathological type of glomerulopathy is determined by renal biopsy will benefit treatment and prognosis, but it find more is essential to evaluate the value and DNA Damage inhibitor risks of renal biopsy and to select an appropriate puncture site via imaging. The right renal lower pole is generally the best site for normal kidneys, but the bilateral lower renal poles of HSK are close to the abdominal aorta, and thus, the upper poles may be relatively more secure

than the lower poles. There have been some case reports about the occurrence of glomerulopathy in HSK in the literature. It is believed by the authors of these reports that the co-occurrence of HSK and glomerulopathy may be a coincidence or HSK can predispose glomerular diseases because it facilitates immune complex deposition and amyloid formation.[6-13] But

because few patients with HSKs receive a renal biopsy, there is a lack of evidence elucidating the causal relationship of glomerulopathy and HSK.[10] We appeal for further study to identify the relationship between horseshoe kdieny and glomerulopathy. We conclude that glomerulopathy as immunoglobulin A nephropathy is a possible explanation for the association of HSK with heavy proteinuria. Renal biopsy may be valuable for HSK patients with heavy proteinuria to identify the type of glomerulopathy MRIP and facilitate further treatment. Moreover, renal biopsy performed by experienced doctors at the renal upper pole using a standard needle biopsy gun under renal ultrasonic guidance may be viable. However, it is necessary to sufficiently evaluate the value, risk and appropriate puncture site before renipuncture. After percutaneous renipuncture, it is also crucial to pay close attention to potential postoperative complications, especially massive haemorrhage. This work was supported by a grant (2011CB944004) from the National Basic Research Program of China, a grant (2012AA02A512) from 863 program and a grant (2011BAI10B00) from the Twelfth Five-Year National Key Technology R&D Program of China. All the authors declare no competing interests. “
“Polyomavirus BK nephropathy (BKVN) is an important infectious complication in kidney transplantation.