T cells isolated from B6 Selleck R788 mice were resuspended with cRPMI at a density of 5 × 106/ml and then incubated for 4 h in vitro with IL-2 (Sigma Corporation, Santa Clara, CA, USA) at a final concentration of 50 U/ml at 37°C in 5% CO2. RNA isolation and first-strand cDNA synthesis were performed as described previously [28]. Primers used for PCR amplification are as follows: for SOCS3, 5′-TGC

GCC ATG GTC ACC CAC AGC AAG TTT-3′ and 5′-GCT CCT TAA AGT GGA GCA TCA TAC TGA-3′. Amplification was carried out for 30 cycles of denaturation for 30 s at 95°C, annealing for 30 s at 60°C, and extension for 30 s at 72°C. After the 30th cycle, the samples were subjected to a final 10-min extension at 72°C. PCR-amplified fragments were fractionated on 1·5% agarose gels and stained with ethidium bromide. Real-time PCR was performed on a LightCyclerTM real-time PCR sequence detection system (Roche, Switzerland), as described previously, Selleck PD0325901 with the following forward and reverse primers, respectively: for SOCS3, 5′-CAA GTC ATC ACT ATT GGC AAC GA-3′ and 5′-CCC AAG AAG GAA GGC TGG A-3′; for β-actin, 5′-CCA GCC ATG TAC GTT GCT ATC-3′ and 5′-CAG GTC CAG ACG CAG GAT GGC-3′. PCR parameters were recommended for the TaqMan Universal PCR Master Mix kit (Applied Biosystems, Carlsbad,

CA, USA). Triplicate samples of twofold serial dilutions of cDNA were assayed and used to construct the standard curves. Lymphocyte proliferation assays were performed as detailed elsewhere [29]. Briefly, freshly isolated B6 naive CD4+ T cells at a density

of 5 × 106/ml were pre-incubated with IL-2 at a final concentration of 50 U/ml Atazanavir for 4 h, and were then stimulated for 72 h with the same quantity of mitomycin-inactivated BALB/c spleen cells at 37°C in 5% CO2. We added the WST-8/Cell Counting Kit-8 (CCK-8 kit, Japan) for 4 h before stopping stimulation with allogeneic antigen, and then detected the optical density (OD) value with a 450 nm microplate reader. Mouse SOCS3 DNA fragments flanked by BamHI and EcoRI restriction sites were generated from a pMD18-T/SOCS3 plasmid obtained in a preliminary experiment by PCR amplification using the primers (5′-CTG GAA TTC ATG GTC ACC CAC AGC AAG TT-3′ and 5′-CTG GGA TCC TTA AAG TGG AGC ATC ATA CTG ATC-3′) targeting the SOCS3 construct. The fragments were cloned directionally into the BamHI and EcoRI sites of a pLXSN vector (kindly provided by the Laboratory of Immunity, Fudan University), and the identity of the product was confirmed by sequencing. PA317 packaging cells were transfected with pLXSN-SOCS3 (2·0 µg/ml) using LipofectamineTM 2000, according to the manufacturer’s instructions (Invitrogen, Portland, OR, USA), and cultured to generate supernatants containing retrovirus.

The majority of patients (93.0%) were waiting for kidney transplantation. More than half of the respondents (63.3%) had been waiting Vemurafenib chemical structure for more than 3 years. Patients with longer transplant waiting times had lower self-estimated chance of receiving a transplant (P = 0.004). Self-estimated chance of getting transplanted

was positively associated with the happiness score (P < 0.0001). Issues of most concerns to the patients waiting for organ transplants were: inconvenience of therapy (48.2%), disease progression (47.9%), burden to family (59.5%) and financial difficulties (52.3%). More female patients on the waiting list (50.0% vs 25.7% in male) reported concerns about suffering associated with the illnesses. 21.7% of patients considered

the level of support received inadequate. Conclusions:  Our patients had long waiting time for transplantation, which is associated with a lower perceived chance of getting a transplant. Attention to more psychosocial support to these patients waiting for organ transplant is important. Promoting and improving organ donation would be the ultimate way to help these patients. “
“Aim:  The prognosis for HIV patients needing acute dialysis is uncertain. The aim of this study was to describe the clinical presentation, renal diagnoses and outcomes of HIV patients who underwent acute haemodialysis at Groote Schuur Hospital in the period 2002–2007. Methods:  A retrospective review of case records of HIV patients who underwent acute haemodialysis was conducted. Results:  buy Palbociclib PAK5 One hundred and seventeen patients were reviewed (median age 34.0 years (29.0–40.0) 53.8% men, 93.2% black Africans) and 33 had a renal biopsy. Acute tubular necrosis (ATN) was diagnosed in 68 patients. Recovery of renal

function occurred in 33.3% of all patients while in 25.7% treatment was withdrawn and 41.0% died in hospital. Suspected ATN was the commonest cause of renal disease in those who recovered renal function (82.1%). A higher CD4 count (odds ratio (OR) = 0.994, P = 0.007), lower pre-dialysis serum creatinine (<1230 µmol/L) and longer hospitalization (OR = 0.93, P = 0.006) significantly correlated with survival. Conclusion:  There is a good chance of survival for HIV patients needing acute dialysis when the diagnosis is ATN, and when the CD4 count is more than 200 cells/mm3. "
“While darbepoetin alfa (DA) can be administered once monthly (QM) to maintain haemoglobin (Hb) concentrations in anaemic patients with chronic kidney disease not on dialysis (CKD-ND), the QM use of DA for anaemia correction has not been previously investigated. In this randomized, double-blind, non-inferiority, active-controlled study, adult subjects with CKD-ND, Hb levels <10 g/dL, and not treated with an erythropoiesis-stimulating agent were randomized 1:1 to receive DA every 2 weeks (Q2W) or QM for 33 weeks with initial doses of 0.75 μg/kg Q2W or 1.5 μg/kg QM.

Inheritance of protective NK KIR3DL1high and KIR3DS1 receptor alleles have also been observed to be over-represented in a high-risk cohort of HESN intravenous drug users and HESN partners of HIV-1-infected subjects. Other intrinsic mechanisms of

innate immune protection correlated with resistance in HESN subjects include heightened dendritic cell responses and increased secretion of anti-viral Buparlisib supplier factors such as β-chemokines, small anti-viral factors and defensins. This review will highlight the most current evidence in HESN subjects supporting the role of epithelial microenvironment and the innate immune system in sustaining resistance against HIV-1 infection. We will argue that as a front-line defence the innate immune response determines the threshold of infectivity that HIV-1 must overcome to establish a productive infection. From the earliest

selleck chemical days of the human immunodeficiency virus (HIV)-1 epidemic, anecdotal evidence of high-risk HIV-exposed but persistently uninfected individuals generated hope that natural resistance to HIV-1 existed in some individuals. The description of persistently seronegative prostitutes in Nairobi, Kenya who maintained resistance to HIV-1 infection despite numerous years of high-risk activity confirmed that resistance to HIV-1, although rare, was possible [1]. This early interest led to the recruitment of HIV-exposed but -seronegative individuals into geographically diverse cohorts of high-risk subjects based upon the route of exposure to HIV-1 (Table 1). Mucosal exposure to HIV-1 in the absence of infection was documented in numerous cohorts from across the

globe, including commercial sex workers [1,2] and individuals practising unprotected heterosexual or homosexual sexual intercourse with an HIV-1-infected partner [3–7]. Importantly, the phenotype of vaginal [8] and rectal [8,9] mucosal resistance to infection in the absence of adaptive T cell responses has been recapitulated in low-dose simian immunodeficiency virus (SIV) rhesus macaque studies, where macaques remained uninfected even after multiple mucosal exposures to SIV, and yet could be Diflunisal infected if virus was given intravenously (i.v.). The absence of vertical transmission has been observed in children born to HIV-1-infected mothers and exposed to HIV-1 through natural birth and/or breast feeding [10–13]. Resistance to infection despite direct blood-borne exposures to HIV-1 were also seen among HIV-seronegative occupationally exposed health workers [14], haemophiliacs receiving tainted blood products [15,16] and i.v. drug users sharing needles [17–20]. The potential diversity of the exposure routes and varied epidemiological background of HIV-1 exposed, uninfected subjects initially complicated the creation of a unifying definition for these seemingly resistant individuals [21].

8 years at age 60) and increasing. Further analysis is required to better define the relationship between improving survival in the dialysis and general populations. 237 THE PREVALENCE AND IMPACT OF PRURITIS IN A DIALYSIS POPULATION J HOLT1,3, S HERATH1, A LEE1,2, K MURALI1,3, M LONERGAN1,2,3, K LAMBERT1 1Wollongong Hospital, NSW; 2Shoalhaven District Memorial Hospital, Nowra, NSW; 3Shellharbour Hospital, NSW, Australia Aim: To

determine the prevalence and impact of pruritis in our dialysis population. Selleck MK-1775 Background: Itching is very common in patients who are on dialysis. Literature regarding the impact of pruritis on quality of life and intensity of itch is limited. Methods: The project was designed as a questionnaire.

Local Ethics approval was obtained. All patients on dialysis for ≥ 3 months area wide were eligible to participate. Participants were approached by an investigator and asked a series of questions. Routine blood results and lists of medications were also recorded. Participants were asked to rate their itch in 3 different ways: Visual Analogue Scale Lund Browder chart to estimate total body surface area involved Impact of itch on quality of life Results: 127 patients were recruited over a 3 month period.114 patients were on haemodialysis and 13 patients on peritoneal dialysis. The mean dialysis vintage was 66.9 months and the mean XL765 duration of HD per week was 14.6 hours. 83 patients reported suffering with itch (63%) and, of these, only 35 (42%) had informed their renal physician. The mean Visual Analogue reading was 31.7 and this method of rating itch did not correlate with any of the usual biochemical parameters. The mean body surface area involved was 18% and did not correlate with the analogue reading. The presence of itch significantly impacted on the ability to fall asleep, pentoxifylline a person’s appetite and their mood, with 69% reporting feeling

unhappy either all or most of the time. Conclusions: Itch is common in patients undergoing dialysis and has a significant impact on quality of life. The majority of patients do not report their symptoms. 238 NEUTROPHIL-LYMPHOCYTE RATIO AS A MARKER OF INFLAMMATION AND PREDICTOR OF MORTALITY IN PATIENTS WITH END-STAGE KIDNEY DISEASE BL NEUEN1, N LEATHER2, A GREENWOOD2, R GUNNARSSON2, JP KILLEN1, RA BAER1, A NIGAM1, I ISMAIL1, L BERLUND1, ML MANTHA1 1Department of Renal Medicine, Cairns Hospital, Cairns, QLD; 2School of Medicine and Dentistry, James Cook University, Cairns, QLD, Australia Aim: To examine the value of neutrophil-lymphocyte ratio (NLR) as a marker of inflammation and predictor of all-cause mortality in patients with end-stage kidney disease (ESKD). Background: NLR is a marker of systemic inflammation that has been shown to predict mortality in patients with coronary and peripheral vascular disease. In contrast to albumin, NLR is unlikely to be affected by nutritional status. Its prognostic value in ESKD patients is unclear.

For human RAG2 expression, the following primers were used: 5′-CAC AGT CAT AGT GGG CAG TCA-3′ and 5′-TGA TGG TAC GTA GAT TTT TGT CTG A-3′. Quantification of the transcript was performed by real-time PCR on an ABI Prism 7000 light cycler (Applied Biosystems, Zug, Switzerland) using SYBR green PCR MasterMix (Fermentas). Ct values were normalized against GAPDH and fold induction was calculated as . We thank Professor Small molecule library mouse Andera Biondi and Dr. Grazia Fazio, Centro Ricerca Tettamanti, Clinica Pediatrica Universitá di Milano-Bicocca, Ospedale San Gerardo, Monza, MI, Italy for providing

the human BM samples. We thank Professors Rod Ceredig and David Nemazee for critical reading of the manuscript. Antonius G. Rolink is the holder of the chair in Immunology endowed by F. Hoffmann-La Roche Ltd., Basel. This work was supported by a grant from the Swiss National Science Foundation to A. G. R. Conflict of interest: The authors declare no financial or commercial conflict of interest.

“
“DGGE of 16S rDNA is one of the most frequently used methods to study microbial communities. In this study, the DGGE profiles of different 16S rDNA regions of the periodontal pathogens Porphyromonas gingivalis, Fusobacterium nucleatum, and Prevotella nigrescens were investigated. The results suggested that V3-V5 and V6-V8 fragments may be suitable for community analysis of subgingival bacteria. Further analysis of subgingival samples with V3-V5 and V6-V8 regions as target fragments suggested that, in chronic periodontitis, PR-171 supplier re-colonization by periodontal bacteria with a population very similar to the baseline may occur by 6 weeks after mechanical debridement. Periodontal infection is initiated by invasive periodontal pathogens in subgingival plaque biofilm.

The first step in periodontal therapy is to alter or eliminate the bacterial communities PtdIns(3,4)P2 responsible for the infection (1). Mechanical debridement significantly improves clinical parameters and is necessary for successful periodontal treatment. However, the data from studies of the effects of periodontal therapy on the subgingival microbiota are confusing (2, 3). So far, several 16S rDNA-based methods have been used for analysis of the effect of mechanical debridement on subgingival bacterial communities. Species-specific regions in 16S rDNA have been used to design primers for PCR analysis to identify unique periodontal pathogens such as Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola (4–6). In addition, PCR primers designed by conserved sequences of 16S rDNA have also been used for amplification of 16S rDNA fragments from all bacterial species found in periodontal pockets. Further separation and analysis of PCR amplicons can profile the bacterial communities of subgingival plaque and elucidate microbial population dynamics (7–9).

The I-PSS total score and nocturnal urine volume significantly improved only by furosemide

treatment. Pirfenidone Conclusion: Furosemide treatment definitively improved nocturia with nocturnal polyuria. GJG treatment may also induce mild improvement of nocturnal polyuria, although further study is required to confirm its efficacy. “
“The purpose of our study was to evaluate the effect of alfuzosin and tadalafil as combination therapy compared with each monotherapy, in patients with lower urinary tract symptoms (LUTS) due to benign prostatic hyperplasia (BPH). Men over the age of 50 years with LUTS secondary to BPH and an International Prostate Symptom Score (IPSS) 8 or higher, were randomized to receive 10 mg alfuzosin (n = 25), 10 mg tadalafil (n = 25) or the combination of both the drugs (n = 25) once daily for 3 months. Symptoms were assessed at baseline, 6 weeks Panobinostat and 3 months. The primary endpoint was the change in IPSS from the baseline. Secondary endpoints were changes in IPSS storage and voiding subscores, peak urinary flow rate, residual urine volume, IPSS quality of life score and erectile domain score. There were significant

improvements in all IPSS scores, peak urinary flow rate and IPSS quality of life score from baseline at both 6 weeks and 3 months in all the three groups (P < 0.003). Combination therapy was better than monotherapy in improving IPSS scores and reducing post-void residual urine volume (P < 0.005). Combination therapy was similar to alfuzosin regarding improvement

in maximum urine flow rate (P = 0.22), similar to tadalafil in improvement on erectile function (P = 0.22) and better than each monotherapy in improving the IPSS quality of life (P ≤ 0.015). Alfuzosin and tadalafil combination therapy provides greater symptomatic improvement as compared to either monotherapy in men with LUTS due to BPH. Benign prostatic hyperplasia (BPH) is a common disease of ageing men. It is clinically characterized by the progressive and bothersome developmentof lower urinary Nintedanib (BIBF 1120) tract symptoms (LUTS). The incidence of moderate to severe LUTS in a large prospective cohort of United States men was about 44% and the progression rate was about 26.5%.[1] Currently, alpha-blockers and 5α-reductase inhibitors (5ARIs) represent the most effective treatment options for BPH. Although these drugs are effective, they are associated with side-effects, which include dizziness, hypotension and sexual dysfunction. These side-effects may be exacerbated by combination therapy. Erectile dysfunction (ED) and LUTS associated with BPH generally begin when men are in the fifth or sixth decade of life and become more common with increases in age. Regular sexual activity is normal in aging men and satisfaction with sex life is an important dimension of quality of life.

Immune cells in the pre-menopausal FRT exist in an environment that is continuously exposed to changing levels of sex hormones. As previously described, several

antimicrobials in CVL or CVM vary with stage of the menstrual cycle. However, the contribution of individual cell types within the FRT toward total antimicrobial production remains relatively understudied with the bulk of research being performed on FRT epithelial cells. As seen in Table IV, we and others have isolated purified uterine epithelial and stromal cells from hysterectomy patients. Under estradiol stimulation, selleck screening library uterine epithelial cells upregulate the production of SLPI, HBD2 and Elafin.72,77 However, the antimicrobial profile of human uterine stromal cells and their response to hormonal stimulation is unknown. In the lower FRT, we observed a very different

response, with vaginal epithelial cells decreasing the secretion of HBD2 and Elafin after 48 hrs of estradiol treatment (Patel et al. unpublished observation). Inhibition progressively increases from 10−8 to 10−10m. In our system, uterine epithelial cells were strong constitutive producers of MIP3α38– an antimicrobial absent from vaginal epithelial cell cultures (Patel et al. unpublished observation). Thus, the vaginal compartment possesses markedly dissimilar responses compared to the uterus – possibly the result of their different embryonic origins, or the differential expression of Endocrinology antagonist co-activator molecules in epithelial cells. Estradiol can also modulate innate immune responses to pathogenic stimuli. For example, estradiol inhibits the LPS-mediated upregulation of IL-6 in uterine epithelial Phospholipase D1 cells.72,77 Whether estradiol influences antimicrobial production in a similar manner remains unknown. The effects of progesterone upon epithelial cells are less well studied (Table IV). We found that progesterone has no effect on HBD2 and Elafin production by fresh primary human vaginal epithelial

cells (Patel et al. unpublished observation). Endometrial explants from the proliferative or secretory phase show a differential response to progesterone. Proliferative phase tissue decreased the mRNA production of HBD1 and HBD2 but increased SLPI in response to progesterone (10−6 m).78 In contrast, no progesterone effect was observed with secretory tissue. As neither estradiol nor progesterone exists alone in the FRT, further studies are needed to investigate the combined effects of these hormones to more accurately represent the in vivo environment. Studies on immune cells recovered from the FRT are limited. It is essential to understand the effects of hormonal stimulation on these cells, as they are a rich source of antimicrobials. For example, neutrophils contain high concentrations of alpha defensins in their granules and are present in greater numbers in the upper FRT during ovulation.

Fourteen patients (64%) with kidney involvement achieved remission, and in seven patients (50%), no flare was seen during the follow-up period. Three patients had renal flare and were successfully re-treated with RTX. Seventeen patients had disease symptoms from airways and eyes at RTX initiation, whereas only 29% displayed ≥50% treatment response. Limited clinical improvement was seen in patients with endobronchial lesions and trachea-subglottic granulomatous disease. RTX is a potent therapeutic

option for ANCA-associated vasculitis refractory to conventional treatment. Best response may be expected in patients with vasculitic manifestations. Granulomatosis with polyangiitis (GPA), previously known as Wegener’s granulomatosis,

is a life-threatening systemic autoimmune vasculitis NVP-BGJ398 characterized by a necrotizing, granulomatous inflammation that predominantly involves upper airways, lungs and kidneys. The disease involves RG7420 datasheet small and medium-sized vessels and is frequently associated with antineutrophil cytoplasmic antibodies (ANCA) recognizing proteinase-3 (PR3). The presence of cytoplasmic ANCA is observed in the majority of patients with active disease, and ANCA titre correlates often with the severity of the disease and response to treatment [1]. In vitro, ANCA causes neutrophil activation, resulting in a respiratory burst and the release of inflammatory cytokines. In a mouse model, the transfer of ANCA specific for MPO causes crescentic glomerulonephritis and small-vessel vasculitis [2], suggesting that ANCA-producing B cells may be directly involved in the disease pathogenesis as precursors of plasma cells producing ANCA [1, 3, 4]. Untreated, the disease usually progresses from a limited necrotizing granulomatous process Rolziracetam to a generalized vasculitis and leads

to fatal outcome in >90% of patients in 2 years with mean survival time of 5 months [5]. The advent of cyclophosphamide (CYC) therapy together with corticosteroids for the induction of remission has reduced the mortality greatly and has become a conventional treatment option of GPA. Although this therapy remains the most effective initial treatment for the active disease, this regimen is associated with toxicity, increased rate of severe infections and dose-related increases in rates of haematological and solid organ malignancies [6]. For this reason, several other immunosuppressive agents, including methotrexate, azathioprine, mycophenolate mofetil, have been used to maintain remission. Unfortunately, in up to 10% of patients, disease is refractory to conventional therapy [7]. Rituximab (RTX) is a chimeric monoclonal antibody directed against the CD20 antigen found on the surface of B lymphocytes. It induces 98% depletion of peripheral blood B cells, but only 40–70% of lymph node B cells are depleted [3].

We report a case

of unusual hemangioblastoma in a middle-aged man with von Hippel-Lindau disease. Neuroimaging revealed multifocal gadolinium-enhancing masses were located within both sides of the cerebellar hemisphere. Histologically, only small areas showing the typical morphology of hemangioblastoma find more were recognized in masses. Most areas of masses were composed of cohesive epithelioid tumor cells with abundant cytoplasm and distinct boundaries. Epithelioid tumor cells were arranged around blood vessels, exhibiting perivascular anuclear zone structures like ependymoma. The epithelioid tumor cells were diffusely positive for vimentin, CD99, neuron-specific enolase, GFAP and focally positive for epithelial membrane antigen (EMA) and D2-40 in a dot-like pattern. Variable-sized lipid droplets and glycogen particles were noted in the cytoplasm of epithelioid tumor cells under an electron microscope. A diagnosis of epithelioid cellular hemangioblastoma with possible ependymal differentiation (WHO grade I) was made. To our knowledge, only a few cases of hemangioblastoma show epithelioid appearance or EMA immunoreactivity. The present case indicates that the stromal cells of hemangioblastoma might originate from primitive neuroectodermal cells,

and they have the capacity to show a distinctive sign of glial or ependymal differentiation. “
“D. J. Bonda, V. P. Bajić, B. Spremo-Potparevic, G. Casadesus, X. Zhu, M. A. Smith and H.-G. Lee (2010) Neuropathology and Applied Neurobiology36, 157–163 Cell cycle aberrations ABT-263 order and

neurodegeneration The cell cycle is a highly regulated and fundamental cellular process that involves complex feedback regulation of many proteins, and any compromise to its integrity elicits dire consequences for the cell. For example, in neurodegenerative diseases such as Alzheimer disease (AD), evidence for abnormal cell cycle re-entry precedes other hallmarks of disease and as such, implicates cell cycle aberrations in the aetiology of AD. The mechanism(s) for Molecular motor cell cycle re-entry in AD, however, remain unclear. Current theory suggests it to be part of a combination of early events that together elicit the degenerative pathology and cognitive phenotype consistent with the disease. We propose a ‘Two-Hit Hypothesis’ that highlights the concerted interaction between cell cycle alterations and oxidative stress that combine to produce neurodegeneration. Here, we review the evidence implicating cell cycle mechanisms in AD and how such changes, especially in combination with oxidative stress, would lead to a cascade of events leading to disease. Based on this concept, we propose new opportunities for disease treatment. “
“Meningeal hemangiopericytomas (HPCs) are aggressive dural-based tumors, for which no prognostic or predictive marker has been identified. Gross total resection is treatment of choice, but not easily achieved; hence, alkylating agents like temozolomide (TMZ) are now being tried.

Due to the progressive involution of thymic tissue, ageing of the T cell compartment in healthy individuals is associated with decreased numbers of circulating naive T cells. This coincides with an increased differentiation status and proliferative history of memory T cells. The process of immunological T cell ageing is related to an age-related decline in cellular immunity, resulting in reduced vaccination efficacy, enhanced susceptibility for infectious diseases and a higher risk for the development of tumours [1-5]. Higher numbers of differentiated CD4+ T cells have also been associated with a higher prevalence

and severity of atherosclerotic https://www.selleckchem.com/products/sotrastaurin-aeb071.html disease [6-9]. We recently documented that patients with end-stage renal disease (ESRD) have

a profound prematurely aged T cell system which is believed to be caused by the uraemia-induced proinflammatory conditions [10, 11]. The immunological age was determined using three parameters: thymic output of newly formed T cells, the differentiation profile of T cells and their relative telomere length. The thymic Selleckchem GSK2118436 function can be measured by T cell receptor excision circles (TREC), which are small circular DNA episomes created in T cell precursors that are formed in the thymus during rearrangement of T cell receptor (TCR) genes [12] and the expression of CD31 on naive T cells [10]. Based on these parameters, the average immunological age of T cells in ESRD patients is 20–30 years higher than that of healthy individuals [10]. Because infection with cytomegalovirus (CMV) has a profound effect on the circulating T cell compartment

in healthy individuals, CMV has been implicated in immunological ageing. For instance, CMV-infected individuals (CMV-seropositive) have a more differentiated memory T cell Niclosamide compartment, a decreased CD4/CD8 ratio, an expansion of CD4+ and CD8+ T cells lacking CD28 but expressing CD57 [7, 13-15] and a reduction in their T cell telomere length, indicating an increased proliferative history of the T cells [16]. These effects of CMV on the T cell compartment are relevant, as a large population of healthy individuals is infected with CMV [17]. The prevalence ranges between 30 and 100%, increases with age and is dependent upon an individual’s socio-economic and ethnic background [8]. More than 70% of ESRD patients are CMV-seropositive, and we have shown previously that a seropositive CMV status is associated with an increased differentiation status of the T cells as determined by phenotyping of the T cell compartment [7, 14]. However, no information is available on other parameters of immunological ageing, such as TREC content, recent thymic emigrants and telomere length, in relation to CMV serostatus in ESRD patients. In this study we tested the hypothesis that CMV infection in ESRD patients may play an important role in all aspects of premature immunological ageing of the T cell compartment.