Both adaptive and innate immune effector mechanisms are believed to contribute to tissue disease aetiology. HLA-E is a non-classical MHC class Ib molecule that acts as the ligand for the NKG2A inhibitory receptor present on natural killer (NK) and CD8+ cells. Peptide binding and stabilization of HLA-E is often considered to signal infection or cell stress. Here we examine the up-regulation of HLA-E in MS brain tissue. Expression is significantly increased in white matter lesions in the brain of MS patients compared with KU-60019 molecular weight white matter of neurologically healthy controls.

Furthermore, using quantitative immunohistochemistry and confocal microscopy, we show increased HLA-E protein expression in endothelial cells of active MS lesions. Non-inflammatory chronic lesions express significantly less HLA-E protein, comparable to levels found in white matter from controls. Increased HLA-E protein levels were associated with higher scores of inflammation. These selleck compound results suggest the potential for an effect in central nervous system pathogenesis from HLA-E modulation in stressed tissue. Co-localization with infiltrating CD8+ cells implicates a possible role for HLA-E-restricted regulatory CD8+ cells, as has been proposed in other autoimmune diseases. “
“Perforin (P) is a prototypical cytotoxic molecule involved in cell-mediated immunity against various pathogens, alloantigens and particularly different tumours. The purpose

of this study was to determine P expression in different lymphocyte subpopulations isolated from

peripheral blood and prostate tissue of patients with benign prostatic hyperplasia (BPH) and prostate cancer (PCa) and compare it with the P expression found in the control group. Twenty subjects were recruited in each of the groups. Prostate mononuclear cells of the BPH and PCa tissues were isolated Fossariinae by enzymatic digestion and gradient density centrifugation, whereas peripheral blood mononuclear cells were isolated by gradient density centrifugation alone. Cells and tissue samples were labelled using monoclonal antibodies against P and different surface antigens (CD3, CD4, CD8 and CD56) and analysed by immunofluorescence and flow cytometry. Total P expression in peripheral blood lymphocytes did not differ significantly between BPH/PCa patients and control group, although the BPH and PCa tissue showed lower P expression level. A negative correlation between prostate-specific antigen levels and the overall percentage of P+, CD3+CD56−P+, and CD3−CD56+P+ cells in the prostate tissue was observed only in patients with PCa. Our findings indicate that the low frequency of P+ lymphocytes, including T, NKT and NK cells, in the prostate tissue of patients with BPH and, particularly, PCa could be the consequence of local tissue microenvironment and one of the mechanisms involved in the pathogenesis of prostate hyperplasia following malignant alteration.

Whole body imaging of adoptively transferred T cells using magnetic resonance imaging, single photon emission computed tomography https://www.selleckchem.com/products/Adrucil(Fluorouracil).html and positron emission tomography techniques, with a focus on regulatory T cells. Clinical and Experimental Immunology 2013, 172: 169–77. Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic synovial inflammation, leading to destruction of joint cartilage and bone. Although the precise aetiology remains to be established, it is thought that RA results from a breach in immune tolerance. T cell responses to several (joint-associated) autoantigens, including ‘altered self’ citrullinated peptides, can be detected in a

proportion of RA patients [1-8], and the function of peripheral blood regulatory T cells (Tregs) is impaired in RA patients with active disease [9]. Immunosuppressive drugs (including biological drugs) can relieve disease symptoms effectively, but none of the currently Akt inhibitor available treatments provide a cure, i.e. a long-lasting and drug-free remission of RA [10, 11]. Moreover, these drugs can increase the risk of serious infections [12-14]. The ‘holy grail’ of the immunotherapy field is

to develop a therapy that targets and rectifies the pathological autoimmune response specifically and effectively, while leaving protective immunity intact. A new immunotherapeutic approach aims to achieve restoration of immune tolerance by treatment with autologous dendritic cells (DC) with tolerogenic function [tolerogenic DC (tolDC)]. Here we review recent progress in this field. Destructive autoimmunity is normally prevented through active silencing of autoreactive T cells, a process in which Ribonucleotide reductase DC play a central role. In the thymus self-reactive T cells are deleted, but this process of ‘central tolerance’ has limitations and some autoreactive T cells escape to peripheral tissues. Here they are kept under control by a variety of mechanisms, termed collectively ‘peripheral tolerance’. When tolerance mechanisms

break down, autoreactive T cells can acquire proinflammatory properties [e.g. become T helper type 1 (Th1) or Th17 cells] and mount an attack on the body’s own tissues, causing an autoinflammatory, destructive immune response [15]. For example, a shift from a tolerogenic to a proinflammatory T cell response in RA has been reported by van Bilsen et al. [3]. They detected CD4+ T cells specific for the autoantigen human cartilage gp39 (HCgp39) in both healthy individuals and RA patients. However, HCgp39-reactive T cells from healthy individuals exhibited a regulatory phenotype [interleukin (IL)-10 production, forkhead box protein 3 (FoxP3) expression, capability to suppress T cell responses], whereas HCgp39-reactive T cells from RA patients produced the proinflammatory cytokine interferon (IFN)-γ and lacked suppressive activity.

Of 902 study subjects, 102

(11.3%) yielded positive hairbrush culture results. Of these, 14 individuals (13.7%) had tinea corporis; the remainder were asymptomatic. Conversion to negative fungal culture was observed in 85 of 96 culture-positive individuals who performed the second hairbrush culture test following Selleck Ku 0059436 treatment. Control of T. tonsurans infection among judo athletes could be achieved by educating athletes, trainers and coaches in judo clubs concerning detection, prevention, and treatment of T. tonsurans infection. “
“A 57-year-old previously healthy woman who works in the fish-processing industry presented with a 1-year history of a slightly pruritic, hyperkeratotic, brownish, erythematous lesion of the left cheek measuring 5 × 5 mm in diameter. Histopathology revealed granuloma formation in the superficial dermal layer by multinucleated giant cells that contained pale-brown septate hyphae.

Periodic acid-Schiff stain showed many hyphae and catenate spores within the multinucleated giant cells. Tissue specimens and skin scrapings Torin 1 solubility dmso were obtained and incubated on mycosel agar, yielding black, velvety colonies that were morphologically identified as belonging to Exophiala species. Sequence analysis of the internal transcribed spacer region of the ribosomal RNA gene showed 99–100% homology to Exophiala oligosperma sequences. This report describes a rare case of phaeohyphomycosis of the face caused by E. oligosperma. “
“We report on an adult patient with tinea capitis caused by Microsporum canis, who presented with diffuse alopecia and follicular pustules, mimicking folliculitis decalvans. Examination 6-phosphogluconolactonase of the scalp showed severe alopecia with prominent involvement of the frontal and vertex scalp: the skin was markedly erythematous with pustules and brownish crusts. Videodermoscopy revealed visible follicular ostia, numerous pustular lesions and several comma hairs. Fluconazole 150 mg a week for 8 weeks associated with ketoconazole shampoo cleared the inflammatory lesions and produced

complete hair regrowth. “
“We report a case of fungaemia resulting from Candida norvegensis in a patient with acute non-lymphoblastic leukaemia-M4 from Turkey. Candida norvegensis was isolated from two different peripheral blood samples that were taken at 2-day intervals. Despite treatment with liposomal amphotericin B, the patient died of multi-organ system failure. “
“There are few reports studying the aetiology of onychomycosis in children in Spain. To study childhood dermatophyte onychomycosis, a retrospective study of children was carried out, who were <16 years of age with dermatophyte onychomycosis diagnosed between 1987 and 2007. Of 4622 nail samples from 3550 patients, 218 came from 181 children up to 16 years old. Onychomycosis caused by dermatophytes was demonstrated in 28 (15.5%) cases.

, 2007). Subsequently, Pal and co-workers demonstrated that Lmp1-deficient spirochetes were severely defective in their ability to persist in murine tissues, especially in the heart, and that Lmp1

deficiency increased B. burgdorferi susceptibility to the bactericidal effects of immune sera in vitro (Yang et al., 2009). Interestingly, Lmp1 mutants survived and persisted in SCID murine tissues, suggesting that Lmp1 is needed to help click here B. burgdorferi resist or evade the host-adaptive immune response (Yang et al., 2009). Lmp1 is a relatively large, 128-kDa surface-exposed protein predicted to contain three distinct domains of similar length: an N-terminal region (Lmp1-N) with no known conserved structural motifs, a middle domain (Lmp1-M) containing seven unique 54-residue repeats, and a C-terminal domain (Lmp1-C) rich in tetratricopeptide (TPR) repeats (Yang et al., 2009). Preliminary studies indicate that the membrane-imbedded region is contained in the N-terminal domain, and in comparison with Lmp1-M and Lmp1-C domains, the immunogenic Lmp1-N domain may be most important for spirochete survival in the murine host (Yang et al., 2010). The functions of the other two Lmp1 domains are currently not well understood, and the significance of the unique Lmp1-M repeats and of the Lmp1-C TPRs is unclear. TPR structures are ubiquitous in prokaryotic and eukaryotic proteins, and they

are specifically involved in protein–protein interactions (Sikorski et al., 1990; D’Andrea & Regan, 2003). Interestingly, IFA data suggest that Lmp1-C, in addition to Lmp1-N, is surface exposed, Nutlin-3 in vivo suggesting that

the C-terminal TPRs may be interacting with host proteins at the B. burgdorferi surface to aid in spirochete survival during mammalian infection. In silico analyses identified BesC (Borrelia efflux system protein C) as a chromosomally encoded ortholog of the E. coli OM channel protein TolC (Bunikis et al., 2008). Protein products of besC (ORF bb0142) and the co-transcribed upstream genes Suplatast tosilate besA (bb0141) and besB (bb0140) are predicted to form a bacterial resistance-nodulation-division (RND)-type protein export system known to be involved in multidrug resistance (Yen et al., 2002; Nikaido, 2003). RND complexes are composed of three protein components: an inner membrane (IM)-localized antiporter protein, a periplasmic membrane fusion protein (MFP), and an OM channel protein, also known as OM factor (OMF; Yen et al., 2002; Nikaido, 2003; Nikaido & Takatsuka, 2009). Bunikis et al. (2008) demonstrated that B. burgdorferi BesC deletion mutants were 2- to 64-fold more sensitive than the wild-type strain to various antimicrobial agents when tested for susceptibility in vitro. Additionally, BesC was found to possess channel-forming activity, with a large conductance of 11 nS in 1 M KCl (Bunikis et al., 2008).

In addition, we analysed pooled bLN fractions for T cell subsets without detecting any differences (data not shown). In summary, no significant differences were identified in CD4+, CD8+ and FoxP3+ Tregs in CD137−/− mice compared with WT mice; these results support our conclusion that CD137−/− mice show an equal Th2-mediated immune response. In our previous work we have shown that administration of an agonistic CD137 mAb inhibited the development of asthma and, moreover, AZD1152-HQPA in vivo was even capable of reversing established airway hyperreactivity (AHR), eosinophilic airway inflammation and production of allergen-specific

IgE in our murine asthma model [21]. Similarly, in a model of atopic conjunctivitis, stimulation of CD137 before or after sensitization inhibited the development of allergic disease [31]. Based on these findings, showing a strong effect of CD137 receptor stimulation in Th2 cell-mediated diseases, we expected

differences when we compared WT and CD137−/− mice in our asthma model. However, in contrast to our expectation, the absence of CD137 signalling did Adriamycin clinical trial not affect the development of allergic asthma; WT and CD137−/− mice developed comparably strong airway eosinophilic inflammation, mucus hypersecretion and enhanced OVA-specific serum IgE levels. The finding that CD137 stimulation via an agonistic mAb had significant effects on the manifestation of allergic parameters [21], whereas missing CD137 signalling did not affect the generation of an allergic phenotype in our model, is difficult to interpret. The potent effect of the CD137 agonistic mAb was associated with reduced production of Th2 cytokines, while secretion of IFN-γ was increased strongly. IFN-γ is one of the main inhibitors of Temsirolimus in vivo Th2 cell development

and cytokine production which play a crucial role in the development and persistence of allergic asthma. Depletion of CD8+ T cells or blockade of IFN-γ partly abolished the protective effect of CD137 agonistic mAb treatment, indicating that this observation was mediated by IFN-γ-secreting CD8+ T cells [21]. This effect is absent in CD137−/− mice, which show comparable Th2 cytokine levels and CD4+ as well as CD8+ T cell frequencies compared to WT mice. In contrast to CD137 triggering the development of Th2 cytokine-producing cells is not affected in CD137−/− mice in our model, which might partly explain the missing difference between WT and CD137−/− mice in our allergic asthma model. Previous reports also show that lack of CD137 signalling does not mandatorily exert opposite results compared with stimulation of this receptor. For instance, treatment with CD137 agonistic mAbs has been shown to exert powerful anti-cancer effects in tumour models, while CD137−/− mice were remarkably resistant to tumour growth [5,7,11]. Follow-up studies demonstrated that CD137 signalling regulates the balance between CD8+ T cells and NK cells via modulation of IFN-γ production.

First-strand cDNA synthesis was performed with the Moloney murine leukaemia virus reverse transcriptase (Promega). The cDNA was amplified with the following primers (sense and anti-sense, respectively):

β-actin (5′-CAGAAGGACTCCTACGTG-3′, 5′-GCTCGTCAGGATCTTCATG-3′, 440 bp), TGF-β1 (5′-ACCTGCAAGACCATCGACAT-3′, 5′-GGTTTTCTCATAGATGGCGT-3′, 279 bp); PCR conditions were initial denaturation at 94° for 3 min then denaturation at 94° for 30 seconds, primer annealing at 60° for 30 seconds, and extension at 72° for 1 min for 35 cycles, followed by SCH727965 cost a final extension at 72° for 10 min. The PCR were size fractionated by electrophoresis on 1·5% agarose gel and visualized by ethidium bromide stain under UV light. The intensity of each band was analysed by densitometry using Scion Image software (Scion Corporation, Fredericle, MD, USA) and the relative mRNA expression of the target gene was normalized to the β-actin

control. Expression of TGF-β1 was assessed by semi-quantitative immunohistochemistry. After being deparaffinized, the section was incubated in 0·01 mol/l citric acid buffer (pH 6·0) for 15 min of microwave antigen retrieval. After cooling, the section was incubated in 3 g/l H2O2 for 30 min (37°), to inactivate the endogenous peroxidase. After blocking by 1 : 10 normal horse serum for 30 min (37°), the supernatant was discarded. Primary anti-mouse selleck TGF-β1 (1 : 400 dilution) was added overnight at 4°. Then, biotinylated goat anti-rat secondary antibody and streptavidin–horseradish peroxidase were

added to the slides and incubated for 30 min at room temperature. Staining was completed by incubation with diaminobenzidine chromogen solution at room temperature. Positive cells Histamine H2 receptor were stained brown and positive signals were the cytoplasm/nucleus brown-stained particles. We used image-pro plus 6.0 to measure TGF-β1 expression intensity. The corrected average optical density was calculated as follows: integrated optical density (IOD SUM) divided by the area of the selected region (area SUM). Total protein was isolated from the right lung by homogenization in a buffer containing 50 mm HEPES (pH 7·4), 1% Nonidet P-40, 0·5% deoxycholate, 5 mm EDTA, 1 mm sodium orthovanadate, 5 mm sodium fluoride, and phosphatase and protease inhibitor cocktails (Sigma-Aldrich). The lysates were centrifuged at 15 545 g for 15 min at 4°, the supernatants were collected, their total protein content was determined using a conventional method, and aliquots were stored at −70° until assayed. Equal amounts of sample proteins were resolved by 10% SDS–PAGE and transferred to a polyvinylidene difluoride membrane by electroblotting in a buffer containing Tris–HCl (25 mm), glycine (192 mm), and methanol (20%, volume/volume).

For example, a mouse model of asthma has demonstrated that the administration of compound screening assay the major allergen of ragweed (Ambrosia artemisiifolia), Amb a 1, linked to CpG ODN reverses airway hyperresponsiveness 36. Two common bacterial species identified in farm cowsheds have been shown to induce a Th1-polarizing program in DC that result in an impaired induction of allergic reactions in mice 37. Evidence also exists from human studies, which support the hypothesis that a balance of Th1/Th2 responses plays an important role in the development of allergy. For example, children with peanut allergy display predominant allergen-specific

Th2 responses, whereas children who outgrow their allergy and children without allergy, show a predominant allergen-specific Th1 phenotype 38. Several clinical trials have also shown that vaccination with Amb a 1 conjugated to CpG ODN inhibited Th2 responses in peripheral blood, eosinophil infiltration in the nasal mucosa and significantly reduce allergic rhinitis symptoms and the need

for medication 39, 40. Recently, https://www.selleckchem.com/products/FK-506-(Tacrolimus).html a new molecular mechanism that explains how DC polarize T-cell responses toward a Th2 or Th1 phenotype has been described 41. The Notch ligand Jagged-1 is constitutively expressed by immature DC and plays an important role in polarizing Th2 responses. Maturation of DC after TLR-triggering by microbial compounds leads to the downregulation of Jagged-1 and upregulation of Delta-4, another Notch ligand playing an important role in the polarization of Th1 immune responses. Over the past oxyclozanide 15 years, an extensive effort has been performed in the phenotypic and functional characterization of nTreg. Nowadays, it is well established that FOXP3 acts

as master switch transcription factor for nTreg development and function 42. In humans, the in vivo relevance of FOXP3 was recognized after the discovery of the X-linked immune dysregulation, polyendocrinopathy syndrome 43. Patients with X-linked immune dysregulation, polyendocrinopathy syndrome present a typical allergic and autoimmune phenotype due to mutations in FOXP3 leading to non-functional nTreg. Similarly, scurfy mice present a deletion in the forkhead domain of FOXP3, which results in an impaired capacity to develop thymus-derived nTreg 42, 45. These mice are characterized by a lymphoproliferative disease, hyper-IgE levels and eosinophilia without a Th2 skewing, with a life-span of approximately 3 weeks. Although there is no direct evidence that allergy is due to impaired function and defects of the FOXP3 pathway, a recent study has shown that single-nucleotide polymorphisms of FOXP3 are associated with allergy development in childhood 44; however, further studies are needed to firmly demonstrate this association.

The isolated CD14+ population had >70% purity as determined by flow cytometry, contaminating cells being mostly CD19+. Monocytes were cultured in serum-free CellGro DC medium (CellGenix, Freiburg, Germany) for 5 days in 24-well plates at 3 × 105 cells per well with recombinant human GM-CSF and IL-4 (R&D Systems, Abingdon, UK; both at 1000 U/ml) to obtain immature DCs. Maturation of dendritic cells.  Maturation of immature DCs was induced by supplementing click here the culture media with the standard maturation cocktail consisting of TNF-α (50 ng/ml), IL-1β (25 ng/ml), IL-6 (10 ng/ml) (all from R&D Systems) and PGE2 (Sigma–Aldrich, Stenheim, Germany; 1 μg/ml).

Alternatively, DCs were matured by adding IFN-α (3000 U/ml), IFN-γ (1000 U/ml), TNF-α (50 ng/ml), IL-1β (25 ng/ml) (all from R&D Systems) and p-I:C (Sigma–Aldrich; 20 μg/ml) to obtain αDC1. DCs were cultivated for 24 h at 37 °C, and immature DCs cultivated without maturation cocktail were used GDC-0449 mouse as controls. When indicated, DCs were pulsed with heat-stressed, necrotic CLL cells at a ratio of 1:1 at the same time as the maturation-inducing cytokines were added. Preparation of heat-stressed necrotic CLL cells as antigen source.  CLL cells were isolated from PBMCs using CD19+ magnetic beads (Miltenyi Biotec). The purity of isolated CLL cells (CD5+ CD19+) was >98%. These CLL cells were resuspended

at a density of 30 × 106/ml in CellGro medium and subjected to heat stress by incubation at 42 °C for 2 h. Heat-stressed cells were then incubated for a further 1 h in 56 °C

and stored in culture medium at −80 °C. When cells were thawed, trypan blue staining showed a cell viability of 0%. Necrotic CLL cells from one patient were used in all experiments. mafosfamide When indicated, a suspension of these heat-stressed necrotic cells was used for the pulsing of DCs. Chemokine determination and immunophenotyping.  For measurement of chemokines, 24 h culture supernatants from previously washed mature DCs were collected and stored at −80 °C until chemokine concentrations were determined by specific ELISAs. When indicated, DCs were pulsed with heat-stressed, necrotic CLL cells at a ratio of 1:1. The commercially available ELISAs for CXCL9/MIG, CXCL10/IP-10, CXCL11/I-TAC, CCL17/TARC and CCL22/MDC (R&D Systems) were performed according to the manufacturer’s instructions. The lower limits of detection were 125 pg/ml for CXCL9/MIG, 62.5 pg/ml for CXCL10/IP-10, 15.6 pg/ml for CXCL11/I-TAC, 15.6 pg/ml for CCL17/TARC and 15.6 pg/ml for CCL22/MDC. For immunophenotyping, fluorochrome-conjugated antibodies anti-CD45 FITC, anti-CCR7 FITC, anti-CD40 PE, anti-CD14 PerCP, anti-CD83 APC and anti-CD86 APC (all from BD Biosciences, San Jose, CA, USA) were added to DCs cultured for 24 h in indicated maturation conditions, incubated at 4 °C for 20 min and washed.

Consider an Australian registry of renovascular intervention versus selleck inhibitor medical therapy. Renal artery vascular disease is increasing in prevalence with the increase in atherosclerosis risk factors such as advancing age, hypertension, diabetes and renal disease1 in the general population. Although this is both large vessel RAS and ischemic small vessel disease, only the former is amenable

to interventional angioplasty. Most authorities consider BP control, preservation or salvage of kidney function and prevention of flash pulmonary oedema to be the goals of treatment of RAS. Optimal medical therapy is considered to be BP-lowering agents, particularly angiotensin converting enzyme inhibitors, antiplatelet agents and lipid-lowering agents. However, angioplasty with stent placement is often now done. The use of distal protection agents are also now more commonly used. Surgical intervention is rarely used, and only in specialized centres. There is no information on the risk of athero-embolic disease after endovascular intervention. This includes peripheral athero-emboli in the feet as well as renal athero-emboli and is not considered in this

document but is referred to in the distal protection subtopic in this series. This document presents a summary of the evidence to date for endovascular treatment and the populations that may benefit, to help guide patient selection for a procedure that Deforolimus has significant peri-procedural morbidity. Databases searched: The terms used to define artherosclerotic renal artery stenosis were ‘renal artery obstruction’ (as a MeSH term and text word) and ‘renal artery stenosis’, ‘renovascular disease$’ and ‘renal artery occlusion$’ as text words. To define this further, the terms ‘atherosclerosis’ and ‘arteriosclerosis’, as both

MeSH terms and text words along with text words ‘angioplasty$’ and ‘stent$’ were searched along with MeSH terms BCKDHB and text words for antihypertensives, flash pulmonary oedema and FMD. MeSH terms and text words for renal artery stenosis were searched for in Medline (1950 to May 2009). The Cochrane Renal Group Trials Register was also searched for trials not indexed in Medline. Date of searches: 10 October 2008, 14 May 2009. There is one systematic review with grading of the evidence up until September 2005 by Balk et al.2 Since this review, one large trial of 806 patients was completed in 2008 (ASTRAL) reported in November 2009 with a median follow up of 34 months making this the largest and longest RCT in the area to date.3 Further large RCTs (>1000 patients) that are due to be published in the next few years include the CORAL study, RAVE study and NITER study.

This then remixes with a known electrolyte concentrate for representation to the dialyser. As the same small water volume can recirculate, at least until column exhaustion, water source independence is assured. Many current technological developments Kinase Inhibitor Library ic50 in dialysis equipment are now focusing on sorbent-based dialysate circuitry. Although possibly déjà vu for some, it is timely for a brief review of sorbent chemistry and its application to dialysis systems. The single pass proportioning dialysis system has been the dominant

haemodialysis configuration since it was commercially introduced in the early 1960s.1,2 Only one other delivery system ever emerged to significantly challenge this method – sorbent dialysis.3,4 However, the cost differential soon heavily biased in favour of single pass delivery paired with reverse osmosis (R/O) water purification. Consequently, by the early 1990s, sorbent dialysis had disappeared from clinical use. Single pass systems are inherently water hungry and, despite solid-state electronics, require regular and costly fluid pathway maintenance. Further, to provide ‘dialysis-grade’

water for the proportioning system, an expensive, complex and power-hungry R/O plant is needed. Even then, the water quality provided by an R/O and single pass system often remains questionable. Late in the either 1990s, interest was rekindled in sorbent-based systems, PLX-4720 manufacturer particularly by those seeking system miniaturization, portability and wearability.5 Meanwhile, the range, capacity and manufacturing costs of dialysis-suited sorbents had also improved. By 2010, although still largely developmental, sorbent dialysis has again emerged as a viable technological alternative.6,7 The search for smaller, portable, water-sparing, low maintenance and user-friendly machines, equally suited to home or to facility, has inevitably led

back towards sorbent technology. A range of new haemodialysis and peritoneal dialysis delivery systems are now basing their independence from continuous-flow water supply on the reconstitution of the dialysate through sorbent cartridges.6–9 This paper seeks to introduce – or reacquaint prior users with – the basic concepts of sorbent-based dialysate regeneration. A sorbent is a material that, either as a solid or a liquid, can bind another substance or compound by adsorption to or absorption into its structure. This bonding may be physical or chemical and, primarily, involves chemical or ionic bonding, or the formation of molecular complexes. The larger the sorbent surface area, the greater the binding efficiency.