Correspondingly, the Register has very few reports of adverse reactions caused by green pea or soy, a substantial number of reports regarding lupin selleck chemicals and fenugreek, and many regarding peanut. These data show that there is a need to further investigate cross-allergy in legumes. Most of the work performed on legume allergy has focused on peanut as the major allergenic legume, and information on other

types of legume allergy is limited [4]. As we previously have established mouse models of lupin and fenugreek allergy [25, 26], we used these models to address the clinical cross-allergy between the four most common allergenic legumes: lupin, fenugreek, peanut and soy. We also assessed different serological and cellular responses to explore possible mechanisms related to the cross-allergic reactions. Animals.  Female inbred C3H/HeJ mice (Jackson Laboratories, Bar Harbor, ME, USA), 5 weeks old at the start of the experiments, were used. Several experiments have been combined in this study and an account of the animals with immunizations and challenges is therefore given in Table 1. Female Sprague-Dawley rats, 150–200 g (Taconic M&B A/S, Ry, Denmark) were used to perform the passive cutaneous anaphylaxis (PCA) tests. The animals were housed, 3–4

mice or two rats per cage, on NESTPAK bedding (Datesand Ltd, Manchester, UK) in type III macrolon cages in filter cabinets (Scantainers), exposed to a 12-hr/12-hr light/dark cycle Unoprostone (30–60 lux in cages), room temperature of 21 ± 2 °C and 35–75% humidity. Pelleted food (RM1; Palbociclib supplier SDS, Essex, UK) and tap water ad libitum were given. Before entering the experiments, the animals were allowed to rest for 1 week. The experiments were performed in conformity with the laws and regulations for experiments with live animals in Norway and were approved by the Norwegian Animal Research Authority under the Ministry of Agriculture. Legume extracts.  The National Veterinary Institute of Norway provided all protein extracts. In short, extracts of peanut, lupin and soy were made by extracting

homogenized peanuts, soybeans or lupin (Lupinus angustifolius) in Tris/glycine buffer, pH 8.7, overnight followed by centrifugation. The fenugreek extract was made using an extended protocol utilizing precipitation with (NH4)2SO4, dialysis and freeze-drying [26]. The total protein concentration of the extracts was measured by Lowry’s method. The endotoxin level of the extract was determined with the Limulus Amebocyte Lysate (LAL) Kinetic-QCL Kit (BioWhittaker, Walkersville, MD, USA) and found to be below 0.1 ng/ml for all extracts. Immunizations and challenges.  Immunizations were performed perorally (p.o.) according to the experimental protocols previously established [25, 26]. Briefly, immunizations were performed on days 0, 1, 2, 7, 21 and 28 and challenges on day 35. Lupin immunized mice received 5.

01 μg/mL anti-CD3ε with graded numbers of MSCs and other reagents as described for individual experiments. Individual experiments were carried out between 2 and 7 times to ensure reproducibility. For culture experiments, individual conditions were generated in replicates of 3–6 and assayed separately. Results were expressed throughout as mean+SD and differences between conditions tested statistically by two-tailed, unpaired Student’s t-test. Significance was assigned at p<0.05. This study was supported by Science Foundation Ireland under grant numbers SFI PI 06/IN.1/B652

(M. D. G), SFI09/SRC/B1794 (M. D. G., J. M. M., F. B., B. P. M. and E. C.), by a Science Foundation Ireland Stoke’s Professorship (R. C.) and by the Health Research Board of Ireland under grant number HRB TRA/2007/04 (O. B.). Conflict of interest:

selleck chemicals llc 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. “
“Ragweed pollen extract (RWE) possesses intrinsic NADPH oxidase activity that induces oxidative stress by initiating the production of intracellular reactive oxygen species (ROS). The this website ROS are important contributors to the manifestation of allergic inflammation; furthermore, concomitant exposure to an allergen and an endotoxin trigger a stronger inflammatory response. One of the main pro-inflammatory cytokines produced in inflammatory responses is interleukin-1β (IL-1β), and its production is associated with caspase-1-containing inflammasome complexes. Intracellular ROS have been implicated in NLRP3 inflammasome-mediated IL-1β production, therefore, we aimed to study whether RWE influences the function of NLRP3 inflammasome. Here we describe that, in the presence

of NADPH, RWE significantly elevates lipopolysaccharide-induced IL-1β production of THP-1 cells as well as human primary macrophages and dendritic cells. We also demonstrate that increased IL-1β production is mediated through NLRP3 inflammasome in THP-1 macrophages. We provide evidence that RWE Meloxicam elevates cytosolic ROS level in these cells, and ROS inhibitors abolish IL-1β production. Furthermore, we show that RWE enhances lipopolysaccharide-induced gene transcription/expression of pro-IL-1β and key components of the inflammasome via a ROS-dependent mechanism. Ragweed (Ambrosia artemisiifolia) pollen is one of the most abundant aeroallergens that cause severe allergic symptoms. After hydration in rainwater, or in conditions with high humidity or moisture, ragweed pollen grains release sub-pollen particles of respirable size.[1] These particles can easily penetrate the lower airways and trigger or exacerbate asthma symptoms.

HSP27 barely co-localizes with tau and with phosphorylated αB-crystallin at Ser59, thus making the formation of active dimers operating as chaperones unlikely. Results suggest a limited function of αB-crystallin and HSP27 in preventing abnormal tau protein deposition in glial cells and neurons; in addition, the expression of αB-crystallin phosphorylated at Ser59 may act as a click here protective factor in glial cells. “
“Inflammatory pseudotumors (IP) are non-neoplastic lesions characterized by collagenous stroma and polyclonal mononuclear infiltrates. It is best characterized in the lung, but can occur in the CNS, mimicking a neoplastic process. We discuss the available literature

and our cases in order to elucidate best medical practices when confronted with such a lesion. We report on two cases of intraventricular

inflammatory pseudotumor in patients who presented with symptoms of CSF obstruction. Both patients were treated surgically with significant clinical improvement. Histopathologically, both specimens revealed a plasma cell granuloma variant of IP. A Medline search for English articles identified 46 cases of CNS IP, only eight of which were located within the ventricle. As with our case, most patients presented due to CSF obstruction or mass effect. Radiographically, the lesions have a variable appearance although most enhanced with gadolinium. Complete resection was achieved in 67% with Trametinib a 12% rate of recurrence. With incomplete resection or biopsy alone, progression is seen despite steroid or radiation administration. Malignant transformation was only reported once. GBA3 CNS IP is a rare pathological entity that cannot be diagnosed through clinical presentation or radiographic characteristics, but rather through a careful neuropathological inspection.

The available literature suggests that complete resection with close follow-up is necessary. “
“The combined 1p-/19q- deletions in oligodendrogliomas originate from translocation between both chromosomes. In the few cases of oligoastrocytomas and glioblastomas with an oligodendroglioma component (GBMO) where only 1p deletion was described, the origin remains unknown. We report the first case of GBMO, in which a single 1p deletion was detected and was linked to a translocation between chromosomes 1 and 7. Fresh surgical specimens were collected during surgery and the samples were used for cell culture, touch preparation smear slides (TP slides) and DNA extraction. Peripheral venous blood was also collected from the patient. G-banding using Trypsin and stained with Giemsa (GTG) banding and karyotyping were performed and 1p-/19q-, TP53, PTEN and c-MYC were analyzed by fluorescent in situ hybridization (FISH). Multicolor FISH (mFISH) and microsatellites analyses were also performed to complete the investigation.

Genetic analysis of various TB proteins has confirmed that MPB64 is identical to MPT64, a protein produced by M. tuberculosis. Non-tuberculous mycobacteria do not produce MPB64; it is specifically secreted by M. tuberculosis complex (17–21). MPB64 was first

isolated by Harboe and Nagai in 1986, whereas Li and colleagues identified it as a secreted protein specific to tuberculous mycobacteria in 1993 (7, 3). Hasegawa and colleagues confirmed the high sensitivity and specificity of the Capilia TB assay, which employs an anti-MPB64 monoclonal antibody to detect MPB64 protein and concluded that this assay was useful for the diagnosis of TB (8). In the present study, we LBH589 concentration assayed urine and serum samples obtained from patients with TB in the active and healing phases by the dot-blot method to assess the profile of reactivity with MPB64 antigen. Rashid and colleagues reported that patients admitted to hospital with TB had a mean ESR 97.04 mm/hr, 57.6% being ≥100 mm/hr (22, 23). In the present study, we investigated the correlation between our dot-blot assay and ESR. In one representative patient, the ESR was around 100 mm/hr one month after commencing treatment and gradually decreased from two months. Our dot blot assays showed that both serum and urine samples paralleled the changes in ESR over time (Fig. Nutlin-3a manufacturer 4a, d, e). All patients with

active TB were positive by dot-blot assay of both serum and urine samples and all patients with a strongly positive result had active TB. Thus, a weak reaction on the dot-blot assay suggests TB and a strong reaction indicates active TB. As shown in Figure 6, analysis that included

data obtained from both TB patients and uninfected individuals revealed a strong correlation between the results obtained by dot-blot assay of urine and serum samples (n = 34, r = 0.672). Analysis of TB patients alone revealed an even stronger correlation between results obtained with urine and serum samples (n = 23, r = 0.841) (data not shown). These findings confirm that the results obtained by assay of urine samples are consistent with those for serum samples. In the present study, we evaluated HAS1 the specificity of a dot-blot test for M. tuberculosis infection by comparing data from infected and uninfected individuals and from patients with active and inactive disease. Moreover, the results obtained from urine samples are closely correlated with those obtained from serum samples. Testing of serum is currently the main method for diagnosis of TB. However, there is a need for an assay kit that allows rapid diagnosis of active TB in the field. In particular, a kit for urine testing would be desirable. Collection of urine requires less skill than does collection of blood, has a smaller risk of contamination and requires no special equipment such as centrifuges. Therefore, urine tests are suitable for mass screening.

To elucidate the role of JAK-3 phosphorylation, we examined the effects of JAK-3 inhibition in cytokine-stimulated rheumatoid synovial fibroblasts in vitro. OSM has been shown to activate synoviocytes to produce proinflammatory mediators, and JAK-3 phosphorylation has been demonstrated in OSM-stimulated Selleckchem Tanespimycin synovial fibroblasts [18]. CP-690,550 is a potent inhibitor of JAK-3, while ICNB028050 is a selective JAK1/2 inhibitor. We therefore examined the effects of JAK-3 inhibition on OSM-induced synovial fibroblasts by comparing their differential effects on JAK/STAT signalling. We stimulated

synovial fibroblasts with OSM to activate JAK1/2/3. OSM stimulation also induced STAT-1/-3/-5 phosphorylation in synovial fibroblasts. CP-690,550 blocked OSM-induced JAK-1/-2/-3 and STAT-1/-3/-5 phosphorylation. Unexpectedly, INCB028050 also inhibited JAK-3 in addition to JAK-1/-2 (Fig. 2). These findings demonstrate that click here CP-690,550 and INCB028050 had similar potencies in terms of suppressing JAK-3, as well as JAK-1/-2 and downstream STAT-1/-3/-5. We assessed the role of JAK-3 in the biological functions of rheumatoid synovial fibroblasts using the JAK-3-specific inhibitor PF-956980 [19]. To evaluate the selectivity of JAK family inhibition, we compared the effects of PF-956980

with CP-690,550 and INCB028050 in OSM-stimulated synovial fibroblasts. As shown in Fig. 3, PF-956980 efficiently blocked OSM-induced JAK-3 phosphorylation,

but had no effect on OSM-induced JAK-1 or JAK-2 phosphorylation in synovial fibroblasts. In contrast, CP-690,550 and INCB028050 blocked JAK-1/-2/-3 phosphorylation in OSM-stimulated synovial fibroblasts. We further examined the effect of JAK-3 inhibition on downstream STATs activation. Selective JAK-3 inhibition caused by PF-956980 prevented OSM-induced STAT-1/-5 activation, but had no effect on OSM-induced STAT-3 activation. In contrast, CP-690,550 and INCB028050 pretreatments blocked activation of all STAT members (STAT-1, -3 and -5) in synovial fibroblasts (Fig. 3). These results suggest that pharmacological JAK-1/-2 inhibition specifically blocks downstream STAT-3 activation, which is involved in the proinflammatory pathway. OSM induces gene expression ADAM7 of cytokines/chemokines or acute phase serum amyloid A (SAA) [20, 21]. To gain insights into the mechanism of OSM signalling leading to induction of MCP-I and acute-phase SAA1/2 gene expression, we extracted total RNA from synovial fibroblasts after treatment with OSM or OSM plus JAK inhibitors for 6 h and subjected it to PCR analysis. As shown in Fig. 4a, PF-956980, CP-690,550 and INCB028050 suppressed OSM-induced MCP-I gene expression. However, although CP-690,550 and INCB028050 also completely blocked OSM-induced SAA1/2 mRNA induction, PF-982560 failed to suppress this induction (Fig. 4b).

6c), thereby ruling out the activation of the IRE1 pathway. Up-regulation of ER chaperones is the hallmark of UPR activation. When assessed by immunoblotting, the caecal and colonic protein samples from the infected mice did not show the induction of BiP, P58IPK or calreticulin as a result Volasertib mouse of infection (Fig. 6d–f). There was no indication of ER chaperone up-regulation at the mRNA level either (data not shown). The phosphorylation of eIF2α and the up-regulation of Il22 in the caeca and colons of C. difficile-infected mice, as well as the up-regulation of Reg3g in their caeca,

raises the prospect of pro-survival signalling in these tissues in response to infection. To investigate this possibility, caecal and colonic protein lysates from untreated and C. difficile-infected mice were probed for the phosphorylation levels of AKT and STAT3. Both the caeca and colons of the infected mice showed a significant increase in AKT (Fig. 7a) and STAT3 (Fig. 7b) phosphorylation levels in comparison to their untreated counterparts. These data support the induction of pro-survival signals in C. difficile-infected mice. This study contains two major novel elements. (i) It analyses the host response in the caeca and colons of C. difficile-infected mice with a panel of > 90 of the genes involved in mucosal biology, and correlates these changes with the cellular response at these sites

of infection, AP24534 order as determined by flow cytometry. (ii) It examines the

induction of the UPR and pro-survival signals at these sites in the aftermath of C. difficile infection. Collectively, the gene expression and flow cytometric results point to four main trends in the local response to C. difficile infection. First, they show an up-regulation of chemokine genes involved in recruiting effector cells of the innate immune response to the sites of infection. CXCL1 and CXCL2 are potent neutrophil chemoattractants and activators, Thymidine kinase and induce neutrophil mobilization from the bone marrow.[43, 44] CCL2 is in turn a chemoattractant for monocytes. Most nucleated cells express CCL2 in response to pro-inflammatory cytokines such as interleukin-1β (IL-1β)[45] or upon engagement of innate immune receptors by a number of microbial products. Flow cytometric analysis had shown a substantial increase in the number of neutrophils in the caeca and colons of the infected mice and up-regulated levels of CD11b on the recruited neutrophils, an indication of their potential activation.[46] It also documented that a higher fraction of cells of the monocyte/macrophage lineage express low levels of MHC II in the caeca and colons of the infected mice, further confirming monocyte recruitment to the site of infection and raising the prospect of their differentiation after exposure to cytokines and/or microbial products.[47] The up-regulation of Cxcl1, Cxcl2 and Ccl2 in the caeca and colons of C.

“
“Please cite this paper as: Bruns, Watanpour, Gebhard, Flechtenmacher, Galli, Schulze-Bergkamen, Zorn, Büchler and Schemmer (2011).

Glycine and Taurine Equally Prevent Fatty Livers from Kupffer Cell-Dependent Injury: An In Vivo Microscopy Study. Microcirculation 18(3), 205–213. Background:  IRI still is a major problem in liver surgery due to warm ischemia and organ manipulation. Steatosis is not only induced by diabetes, hyperalimentation, alcohol and toxins, but also chemotherapy given before resection. Since steatotic livers are prone to Kupffer cell-dependent IRI, protection of steatotic livers is of special interest. This study was designed to compare the effect of taurine and glycine on IRI in steatotic

livers. Materials and Methods:  Steatosis was induced with ethanol Selleckchem Osimertinib (7 g/kg b.w.; p.o.) in female SD rats. Ten minutes after inactivation of Kupffer cells with taurine or glycine (300 mM; i.v.), left liver lobes underwent 60 minutes of warm ischemia. Controls received the same volume of valine (300 mM; i.v.) or normal saline. After reperfusion, white Small molecule library blood cell-endothelial interactions and latex-bead phagocytosis by Kupffer cells were investigated. Liver enzymes were measured to estimate injury. For statistical analysis, ANOVA and Student’s t-test were used. Results:  Glycine and taurine significantly decreased leukocyte- and platelet-endothelium interactions and latex-bead phagocytosis

(p < 0.05). Liver enzymes were significantly lower after glycine and taurine (p < 0.05). Conclusions:  This study shows that preconditioning with taurine or glycine is equally effective in preventing injury to fatty livers most likely via Kupffer cell-dependent mechanisms. "
“Angiogenesis is a multistep process that requires intricate changes in cell shape to generate new blood vessels. IF are a large family of proteins that play an important structural and functional role in forming and regulating the cytoskeleton. Vimentin, a major type III intermediate filament protein is expressed in endothelial and other mesenchymal cells. The structure of vimentin is conserved in mammals and shows dynamic expression profiles in various cell types and different developmental stages. Although initial studies with vimentin-deficient Clostridium perfringens alpha toxin mice demonstrated a virtually normal phenotype, subsequent studies have revealed several defects in cell attachment, migration, signaling, neurite extension, and vascularization. Regulation of vimentin is highly complex and is driven by posttranslational modifications such as phosphorylation and cleavage by intracellular proteases. This review discusses various novel functions which are now known to be mediated by vimentin, summarizing structure, regulation and roles of vimentin in cell adhesion, migration, angiogenesis, neurite extension, and cancer.

10 An additional application has been the use of a protein leaky membrane to treat myeloma kidney with good success.11 Flux, in relation to dialysers, can mean two things. It may relate to the passage of larger molecules – with β2 microglobulin (MW 11 800) commonly used as the marker molecule given its likely

importance in the pathogenesis of DRA. Thus high-flux membranes will allow the passage of β2 microglobulin, whereas low-flux membranes will not. However, flux may also relate to the Kuf of the membrane. Kuf is the ultrafiltration coefficient of the membrane – the rate at which water crosses the membrane at a given trans-membrane pressure. Under the conditions of normal dialysis, there exists a trans-membrane pressure – high-flux membranes allow a greater volume of water to cross the dialysis membrane BMN 673 ic50 per unit time at a given pressure. Low-flux membranes typically have Kuf values below 10 mL/min per mmHg, whereas

high-flux membranes most commonly have values above Trametinib 20. The widespread usage of high-flux membranes was in part responsible for the universal application of ultrafiltration monitors to dialysis machines, as these monitors are a mandatory requirement when using these membranes, otherwise the very large obligatory ultrafiltration loss would volume deplete the patient. The benefits of high-flux membranes are said to lie in several domains. The improved biocompatibility is less likely to cause intra-dialytic symptoms such as hypotension, nausea and headaches; however, supportive data are lacking.12 It is also proposed that the high-flux membranes improve cardiovascular stability, especially during dialysis itself. This may relate to the improved biocompatibility with less induction of cardiovascularly active agents, such as the cytokines and to the potential removal of similar agents (e.g. IL-1 and TNF would both be potentially removed by high-flux membranes).13

However, some claim that this cardiovascular stability relates more to improved temperature balance during dialysis because of greater shifts between blood and dialysate.14 PAK5 Furthermore, the clearance of β2 microglobulin probably reduces the likelihood of the development of DRA – observational data would support this although there are no randomized trials to firmly establish this, although several large observational trials are supportive.15 Certainly, the incidence of DRA seems to have diminished markedly in the last 10–15 years. The reduction in DRA may also relate to the reduced cytokine induction, as cytokines such as IL-1 and TNF are involved in this process. Early observational data suggested that high-flux dialysis was associated with improved survival. For example, Woods reported on the experience in Singapore with conversion of a cohort of patients to high-flux dialysis – with demonstration of a reduction in the mortality rate compared with historical controls.

A statistical comparison is presented in Table 2. When compared with sialolithiasis (non-autoimmune control), VH clones of SS were frequently unmutated (P = 0.0005) as they were with IgG4-related sclerosing sialadenitis (P < 0.0001). For VH3 family clones, rates of unmutated clones in cases of SS and IgG4-related sclerosing sialadenitis were significantly higher than in the sialolithiasis cases (P = 0.002 and P < 0.0001, respectively). In contrast, there were no significant differences in non-VH3 family clones. In our study, we retrieved typical

clinical cases of SS, IgG4-related sclerosing sialadenitis and sialolithiasis. Selleck EPZ-6438 We then analysed VH fragments of B cells infiltrating these three types of lesions. After PCR amplification of rearranged IgH genes, at least 50 clones per case and more than 500 clones in total were sequenced for VH fragments, and the data obtained showed that VH fragments of SS and IgG4-related

sclerosing sialadenitis cases were frequently unmutated. We employed sialolithiasis tissues as a non-autoimmune control and observed chronic inflammation together with many mature lymphoid and plasma cells. In previous VH analyses [17, 18], peripheral blood B cells have been used as a control. However, as about 70% of peripheral blood B cells are naïve or unmutated [19], we consider that local non-specific inflammatory lesions (e.g. those of sialolithiasis) would be a more appropriate control in analysing local inflammation in autoimmune diseases. Hansen et al. reported that the VH3 family was preferentially used in a patient with SS (VH3 > VH1 ≥ VH4 > others) [18]. In this study, a similar VH usage was observed in SS GDC-0973 cell line and IgG4-related sclerosing sialadenitis cases: the VH3 family was the most frequently used and VH3-23 was the most often used among VH3 fragments. However, this usage of the VH3 family and a tendency towards use of VH3-23 was also found in the sialolithiasis controls, suggesting that the VH usage patterns observed in SS and IgG4-related sclerosing sialadenitis were not specific. Most interestingly, VH clones Phospholipase D1 were often unmutated in SS

and IgG4-related sclerosing sialadenitis and the percentage ratios of unmutated/total clones were 30% and 39%, respectively. These rates were significantly higher than that of sialolithiasis clones (14%). In addition, the unmutated clones appeared to be derived mainly from the VH3 family because VH3 family clones were often unmutated in SS (36%) and IgG4-related sclerosing sialadenitis (48%), when compared with those in sialolithiasis (15%). In contrast, when non-VH3 family fragments were analysed, the unmutation ratios were uniformly low (11–16%) in all three lesions. Unfortunately, owing to the small number of clones analysed, we were unable to determine which fragment of the VH3 family contributed most to the higher rates of unmutated clones in SS and IgG4-related sclerosing sialadenitis cases.

Improvements from baseline to end-point were also recorded for grip strength in the dominant hand (treatment difference 10·9 kPa; P = 0·0008) and the non-dominant Silmitasertib price hand (8·6 kPa; P = 0·005). Results were similar during the second cross-over period. During the extension phase, participants who continued to receive IVIG had

a longer time to relapse than did patients treated with placebo (P = 0·011). This is the first study that demonstrates clearly the long-term efficacy and tolerability of IVIG in CIDP. Another recent, multi-centre, randomized, double-blind, placebo controlled, parallel-group study in 45 patients with CIDP compared the efficacy and tolerability of IVIG (0·5 g/kg/day for 4 consecutive days) to intravenous methylprednisolone (0·5 g/day for 4 consecutive days) given every month for 6 months [37]. After therapy discontinuation, patients were followed-up for 6 months to

assess relapses. The primary outcome was the number of patients discontinuing either therapy owing to inefficacy or intolerance. MLN8237 order Secondary end-points included the proportion of patients experiencing adverse events or worsening after therapy discontinuation. More patients stopped methylprednisolone (52%) than IVIG (13%) (P = 0·0085). The reasons for discontinuation were lack of efficacy, adverse events or voluntary withdrawal. After therapy discontinuation, more patients on IVIG worsened and required further therapy (38%) than did those on methylprednisolone (none) (P = 0·0317). Thus, treatment of CIDP with IVIG for 6 months was discontinued less frequently because of inefficacy, adverse events or intolerance than treatment with intravenous methylprednisolone. Another recent prospective, multi-centre, single-arm, open-label Phase III study [Privigen® Impact on Mobility and Autonomy

(PRIMA) trial] evaluated the efficacy and safety of IVIG in 28 patients with CIDP [38]. Patients received one induction dose of IVIG (2 g/kg body weight) and up to seven maintenance doses (1 g/kg body weight) at 3-week intervals. The overall responder rate defined as an improvement of ≥1 point on the INCAT disability scale at completion Calpain was 60·7%. IVIG-pretreated patients demonstrated a higher responder rate than IVIG-naive patients (76·9 versus 46·7%). The INCAT score, the maximum grip strength and the Medical Research Council sum score all improved significantly at completion compared to baseline. Thus, these recent trials provide evidence for the long-term efficacy of IVIG in patients with CIDP. Adverse effects, frequent: headache, hypertension, allergic/anaphylactic reactions [especially in immunoglobulin (Ig)A-deficient patients], dermatitis; infrequent: infection (HIV or viral hepatitis) by contaminated blood product, pulmonary oedema from fluid overload, due to the high colloid oncotic pressure of IVIG, venous thrombosis, aseptic meningitis and haemolysis.