3M-003 produces a cytokine cascade in animals that resembles imiquimod (TLR-7 stimulation), but is a more potent activator of both TLR-7 and TLR-8 receptors than imiquimod (Gorden et al., 2006). The activation of macrophages by an imidazoquinoline resulting in significantly enhanced killing of C. albicans is a novel finding. Presumably, this is mediated via TLR engagement, the signaling pathways mentioned, and induction of the transcription factor NF-κB (Sauder, 2003). Most relevant to the induction of the antifungal activity in macrophages by this drug family are reports of imiquimod-induced macrophage killing of Leishmania donovani (Buates & Matlashewski,

1999, 2001). The authors showed that the killing activity Hydroxychloroquine of imiquimod-activated macrophages was due to upregulation of iNOS and NO production. This in vitro activity correlates with clinical antileishmanial activity (Arevalo et al., 2007). Imiquimod upregulation of iNOS and macrophage NO production is similar to IFN-γ activation of macrophages where iNOS is upregulated and

enhanced NO production is required for antifungal activity, for example against Histoplasma capsulatum (Brummer & Stevens, 1995). Because NO production contributes to the candidacidal activity of activated macrophages (Rementeria et al., 1995; Vazquez-Torres et al., 1996), we proposed that macrophages activated by 3M-003 exert candidacidal activity in a NO-dependent manner. Our data indicate that NO production plays a role in the candidacidal activity of 3M-003- or IFN-γ-activated macrophages. However, the role of NO in killing of C. albicans NVP-BKM120 may be limited, and a full dose–response curve with MMA would be needed to specify the NO contribution. In contrast, NO production played a more substantial

MTMR9 role in killing of H. capsulatum by IFN-γ+LPS-activated macrophages in our hands (Brummer & Stevens, 1995) or L. donovani by imiquimod- or IFN-γ+LPS-activated macrophages (Buates & Matlashewski, 1999). In contrast to the effect of 3M-003 on macrophages, 3M-003 did not significantly directly increase the candidacidal activity of monocytes or neutrophils. We speculate that, as with natural killer cells (Hart et al., 2005), a paucity of TLR-7 and TLR-8 on monocytes and neutrophils from mice might account for the poor responses to 3M-003 for the induction of candidacidal activity. Alternatively, these TLRs may respond differently in these cell types, and a different spectrum of responses, including different cytokines, may be produced. Only one of the three murine neutrophil subsets expresses TLR-7, and only one expresses TLR-8 (Tsuda et al., 2004). Mice do not have the benefit of a fully functional TLR-8 response to this drug family (Gorden et al., 2006). Imiquimod appears to stimulate macrophages through TLR-7 (Hemmi et al., 2002).

Therefore, we investigated if mMCP-1 contributes to schistosomiasis-induced alterations in epithelial permeability and secretion and to egg excretion. Adult male Mcpt-1+/+ (WT) and Mcpt-1−/− BALB/c F10 mice were generated as PI3K inhibitor previously described (19) and were bred at the University of Antwerp (Antwerp, Belgium) under specific pathogen-free conditions. The animals were given food and water ad libitum and were kept in a 12 : 12 h light/dark cycle. All experimental procedures were approved by the local ethics committee of the University of Antwerp. Mice were infected according to the method of Smithers and Terry (20) at 6–8 weeks of age. Briefly, after shaving the anesthetized animals, a heavy metal ring

was placed on the lower abdomen and 1·2 mL water containing 100 freshly shed cercariae of a

Puerto Rico strain of S. mansoni was pipetted into this ring. The animals were exposed for 10 min, allowing the cercariae to penetrate transcutaneously. The cycle of S. mansoni was maintained in the laboratory by passage through Biomphalaria glabrata snails. To prevent variation caused by the infection procedure, in each independent experiment, WT as well as Mcpt-1−/− mice were infected. Mice, infected 6–12 weeks prior to investigation, and age-matched control mice, were killed by GW-572016 purchase cervical dislocation followed by exsanguination. Of all infected animals used in the study, the liver was macroscopically evaluated for the presence of granulomas. In dedicated experiments, adult worms were recovered from the hepatic

portal system and the liver of infected WT (n = 5) and Mcpt-1−/− mice (n = 5) by cardiac perfusion with citrate saline (0·85% sodium chloride, 1·5% sodium citrate) after intraperitoneal injection with an overdose of Nembutal (150 mg/kg) (20). The worms were counted immediately. Infected WT and Mcpt-1−/− mice [6–12 weeks post-infection (w p.i.); n = 7/time point] were allowed to defecate overnight. Single faecal pellets were placed in isotonic saline solution, disrupted by aspiration with a 10-mL syringe and filtered through a 320-μm metal sieve, as previously described (21). Each filtrate was passed through a sheet of Whatman No.4 filter paper and the eggs were stained with saturated Ninhydrin solution (22). Dried papers were examined in triplicate at Buspirone HCl 50× magnification by two independent observers. The results are expressed as the number of eggs/100 mg faecal matter. The ileum of infected WT and Mcpt-1−/− mice (6–12 w p.i.; n = 7/time point) was removed and washed in Krebs solution (in mm: 117 NaCl, 5 KCl, 2·5 CaCl2.2H2O, 1·2 MgSO4.7H2O, 25 NaHCO3, 1·2 NaH2PO4.2H2O and 10 glucose; pH 7·4). One gram (wet weight) of each ileum was digested in 5 mL of a 5% potassium hydroxide solution at 37°C for 16 h (23). Fifty-μL aliquots of the digests were evaluated on microscope slides and the eggs counted at 25× magnification.

These findings suggest that toxicants and environmental stressors associated with MTM negatively affect communities proximal to these mines. As with all mining operations, MTM site operators are required to abate fugitive dust generation in open mine areas [1]. However, abatement is not required for fugitive dust generated by blasting and combustion particulates from heavy equipment. Hence, PM may represent a significant toxicant

generated by active MTM sites [17]. PM mortality has been demonstrated over a wide variety of geographical locales [12]. By source, PM derived from combustion appears to possess the greatest toxicity Seliciclib in vivo of ambient sources [10]. While size is a strong predictor of cardiovascular toxicity [43], coarse PM exposures also have been associated with cardiovascular morbidity and mortality [13]. There is a lack of literature pertaining to PMMTM; however, Selleck H 89 a good corollary can be drawn between PMMTM and PM produced by opencast mining [17, 23]. Opencast mining PM contains largely the geological and mineralogical composition of the mine, and a significant portion of combustion source particulates, with little coal dust in the total sample [23]. Hence, PMMTM used in this study would predictably

contain a great deal of crustal material and combustion source PM, the latter of which a significant database of untoward health effects exists [29, 38]. While this knowledge is critical for making the initial speculations on analogous health outcomes, it does little to illuminate the underlying mechanisms of microvascular relationships. The microcirculation is the primary site of vascular resistance and nutrient and waste exchange in the body. Perturbations in microvascular vasoreactivity can have profound impact on tissue perfusion, and ultimately homeostasis mafosfamide [41]. Deficits in tissue perfusion through microvascular

dysfunction can eventually lead to ischemia. Indeed, several cardiovascular conditions that are ultimately the result of microvascular dysfunction and pathology are angina, myocardial infarction [3], stroke [42], and hypertension [45]. Microvascular dysfunction is probably not isolated to a particular vascular bed, but occurring simultaneously throughout the body [42]. Hence, the complex mechanisms involved in microvascular function that controls tissue specific perfusion are of paramount importance with regard to the systemic microvascular effects that follow PM exposure. Given that tissues probably develop microvascular dysfunction in concert, the purpose of this study was to evaluate underlying mechanisms of arteriolar function in disparate systemic microvascular beds following PMMTM exposure. We hypothesized that PMMTM exposure alters arteriolar reactivity through mechanistic pathways involved in endothelium-dependent arteriolar dilation, particularly NO-mediated dilation, and that these alterations in vasoreactivity would vary by vascular bed.

Conclusion: Treatment of OAB

with solifenacin is associated with significant improvement in generic HRQoL and disease-specific symptoms at 8 weeks after drug administration. selleck chemicals Particularly for generic HRQoL as measured by the SF-36, solifenacin treatment effectively improves three SF-36 scores: PF, VT, and MH. “
“Objectives: It has been reported that nitric oxide (NO) mainly contributes to prostate or urethral smooth muscles relaxation, and that nitrergic innervation and neuronal NO synthase (nNOS) levels are decreased in benign prostatic hyperplasia. The purpose of the present study was to evaluate the feasibility to gene therapy for benign prostatic hyperplasia by transferring nNOS gene into the rat prostate with in vivo electroporation (EP) procedure. Methods: Male Sprague–Dawley rats were divided

into four groups (sham, only EP, only nNOS injection, and nNOS gene injection with EP groups). Fifty micrograms of luciferase gene and nNOS expression vectors in 50 µL of K-PBS (potassium-phosphate buffered saline) were injected into the prostate. Immediately after the injection of these vectors, the vector injection points were electroporated by the two-square parallel check details electrodes. Two days after gene transfer, luciferase analysis and an immunohistochemical staining for nNOS were performed, and NO2−/NO3− (NOX) release was measured using high-performance liquid chromatography coupled with the

microdialysis procedure. Results: The optimal electric pulse conditions were 50 V, 1 Hz and 10 msec. In vivo EP with these conditions showed the increase in the luciferase gene expression approximately 300-fold of the control group. In the nNOS gene injection with EP group, the marked nNOS immunoreactivity was observed, and NOX release was significantly higher, as compared to other groups. Conclusion: The results suggest that EP is a feasible technique for in vivo gene transfer into the rat prostate, and that the transferred nNOS gene functionally expresses and contributes to NO production. “
“Bladder hypertrophy and dysfunction are well-known bladder responses to outlet obstruction (i.e. urodynamic overload). Cardiac hypertrophy and heart failure are also caused by hemodynamic overload, and Loperamide many basic and clinical studies suggest that the local renin-angiotensin system (RAS) has a crucial role in load-induced cardiac pathogenesis. The similarity of the response of the heart and the bladder to overload suggests that angiotensin II (AngII) may have a similar regulatory role in pathological remodeling, such as muscle growth and collagen production of the obstructed bladder. Previous in vitro studies show that angiotensin I is converted to AngII by angiotensin converting enzyme (ACE) or chymase, which exists in the human bladder.

, 2001; Peng et al., 2001; Crabtree & Olson, 2002; Ryeom et al., 2003; Zhu et al., 2003). Calcineurin is especially important in T-lymphocytes. Its stimulation of IL-2 transcription here is a key mediator of T-cell activation and the subsequent autocrine loop

proliferation find more that is so critical to adaptive immune response. This pathway is so important that clinically, it is a major target of immunosuppressants such as cyclosporin A (CsA) and FK506 for transplant and autoimmune patients (Liu et al., 1991, 1992; Schreiber & Crabtree, 1992). Ryeom et al. (2003) investigated the role of RCAN1 in T-cells by assessing the induction of calcineurin-dependent proinflammatory genes in RCAN1-deficient mouse T-lymphocytes. They observed decreased interferon-γ (IFN-γ) production, lower proliferation, and an overstimulation of FasL leading to apoptosis in RCAN1-deficient T-lymphocytes. Also, we observed that the stimulation of Jurkat and primary T-lymphocyte signaling leads to isoform 4 induction in a calcium, calcineurin, and reactive oxygen species (ROS)-dependent manner that is accompanied by IL-2 induction (Narayan et al., 2005). Despite these T-cell studies, however, there has been a surprisingly

lack of reports on the involvement of RCAN1 in immune function. The aim of the presented studies is to further investigate the role of RCAN1 in immune response, extending the above prior studies in T-lymphocytes. Because T-cells are involved in adaptive immunity, Doxorubicin mw we decided to initially ever investigate the role of RCAN1 in the other major defense system, innate immunity, and chose macrophages for these studies. Subsequently, we examined the role of RCAN1 in vivo by assessing the impact of deleting RCAN1 expression on the susceptibility of mice to bacterial (Fransicella tularensis) infection, especially the production of proinflammatory cytokines because calcineurin is an important regulator of these genes. Mouse macrophage RAW 264.7 cells (ATCC) were cultured in Dulbecco’s modified Eagle’s medium plus 10% heat-inactivated fetal calf serum containing 50–100 U mL−1 penicillin and 50–100 μg mL−1 streptomycin, and maintained in a humidified

incubator atmosphere of 95% air and 5% carbon dioxide (CO2) at 37 °C. Mouse primary bone marrow macrophages (BMM) were flushed from 3-month-old WT and KO mice femur bone marrow using RPMI media. After centrifugation, red blood cells were lysed and the bone marrow cells were resuspended in bone marrow media for macrophage differentiation in L-cell-conditioned media for 7 days. After a change of media, the cells were then counted and plated in whole bone marrow media and maintained in a humidified incubator atmosphere of 95% air and 5% CO2 at 37 °C. Cells were grown to 60–80% confluency at the time of agonist addition. These agonist treatments included Escherichia coli lipopolysaccharide, Staphylococcus aureus lipoteichoic acid (LTA), and S. aureus peptidoglycan, all obtained from Sigma (St.

Virulence is a rare outcome of infection, occurring in fewer than 1 in 10 infections. Not all strains of the parasite are equally virulent, and understanding the mechanisms and causes of virulence is an important goal of Entamoeba

research. The sequencing of the genome of E. histolytica and the related avirulent species Entamoeba dispar has allowed https://www.selleckchem.com/products/CP-690550.html whole-genome-scale analyses of genetic divergence and differential gene expression to be undertaken. These studies have helped elucidate mechanisms of virulence and identified genes differentially expressed in virulent and avirulent parasites. Here, we review the current status of the E. histolytica and E. dispar genomes and the findings of a number of genome-scale studies comparing parasites of different virulence. “
“CD4+ T cells expressing the latent form of transforming growth factor-β [latency-associated peptide (LAP) (TGF-β1)] play an important role in the modulation of immune responses. Here, we identified a novel peptide ligand (GPC81–95) with an intrinsic ability to induce membrane-bound LAP (TGF-β1) expression on a subpopulation of human CD4+ T cells (using flow cytometry; ranging from 0·8% to 2·6%) and stimulate peripheral blood mononuclear cells to release LAP (TGF-β1) (using ELISPOT assay; ranging from 0·03%

to 0·16%). In spite of this low percentage of responding cells, GPC81–95 significantly reduced Toll-like receptor 4 ligand-induced tumour necrosis factor-α

production in a TGF-β1- and CD4+ T-cell-dependent BGB324 molecular weight manner. The results demonstrate that GPC81–95 is a useful tool to study the functional properties of a subpopulation of LAP (TGF-β1)+ CD4+ T cells and suggest a pathway that can be exploited to suppress inflammatory response. Transforming growth factor-β1 (TGF-β1) is involved in the regulation of numerous cellular functions and is produced by most cell types in a latent form. The latent form of TGF-β1 [LAP (TGF-β1)] is comprised of latency-associated peptide (LAP) non-covalently bound to mature TGF-β1. It is known that many immune cells can produce LAP (TGF-β1) or can express this molecule on their cell surface1,2 and that LAP (TGF-β1)-expressing CD4+ T cells play an important role in modulation of immune responses.3–5 It has been shown that oral or nasal administration of anti-CD3 MYO10 antibodies induces LAP (TGF-β1)+ CD4+ T cells and suppresses autoimmune disease in animal models in a TGF-β1-dependent manner,3,6 but there is little information on other LAP (TGF-β1)-inducing ligands or the mechanism involved in the induction of this regulatory molecule on CD4+ T cells. Tumour necrosis factor-α (TNF-α) is a pro-inflammatory cytokine that is produced mainly by monocytes and macrophages after stimulation with endotoxin.7 It has many immunostimulatory functions and plays a crucial role in inflammation and immunity.

T helper-1 (Th1) cells are necessary for EAMG development and interferon-γ (IFN-γ) and interleukin-12 (IL-12; the major Th1 cytokines) play a critical role in EAMG development [[5-7]]. Th2 cells secrete a different cytokine profile that confers different effects on EAMG pathogenesis. On one hand, research describing the role of cytokines in the progression of MG and EAMG has revealed that the Th2 cell-related cytokine IL-4 (an efficient growth promoter for B-cell proliferation and differentiation) is important to the development of anti-AChR antibody production [[8]]. On the other hand, IL-4 appears to be involved in

the prevention of the development of EAMG [[9]]. Treg RG-7388 cells that secrete transforming growth factor-β (TGF-β) and down-regulate various T-cell-mediated responses are functionally defective in MG patients [[10, 11]]. Furthermore, the IL-17-producing Th17 Th-cell phenotype has been shown to play

a dominant role in promoting inflammation autoimmunity [[12, 13]] and EAMG [[14]]. Extracellular adenosine is considered to be an essential physiologically negative regulator click here of immune reactions [[15-17]] that initiates transmembrane signaling via 4 G protein-coupled adenosine receptor subtypes designated A1 receptor (R), A2AR, A2BR, and A3R [[18]] and the A2AR is predominantly expressed on T cells [[19, 20]]. The importance of A2AR in mediating adenosine-mediated negative regulation

has been clearly demonstrated in A2AR null mice [[15]] and increased awareness of the role played by both adenosine and A2AR in controlling immune function and inflammation has generated significant Clomifene interest regarding the potential use of adenosine-receptor-based therapies in the treatment of autoimmune-based diseases [[18]]. In addition, recent reports have also indicated the development of A2AR-based treatments for autoimmune diseases such as systemic lupus erythematosus [[21]], Parkinson disease [[22]], and experimental autoimmune encephalomyelitis [[23, 24]]. Methotrexate, an antirheumatic drug, has been shown to modulate anti-inflammatory responses via interactions with the A2AR in vivo [[25]]. Besides, A2AR agonists have been reported to possess inhibitory effects in the context of alloantigen-induced immune responses associated with the attenuation of tissue rejection following skin transplantation [[26]] or hepatic ischemia/reperfusion injury [[27]]. However, the regulatory role of A2AR in mediating EAMG disease severity and progression has not been described. In this study, we investigated whether A2AR expression was functionally altered in rats presenting with EAMG and whether the administration of an A2AR agonist prevented EAMG induction or facilitated improvement of clinical symptoms associated with established disease.

Before the formation of C. albicans biofilm layer on invasive medical devices, yeasts colonize the surface, for example a central venous or urinary catheter. In this step, C. albicans begins to express surface proteins promoting adhesion (Nobile et al., 2008; Soll, 2008). This step is a key to starting to build a biofilm. At this stage, the process of biofilm formation can be influenced very effectively. For example, echinocandins have been confirmed to be applied very successfully to inhibit adherence and reduce biofilm formation (Kuhn et al., 2002; Cateau et al., 2007). Other reports noted the ability of IgG purified

from rabbit serum immunized with C. albicans cytoplasmatic extract to reduce the

capacity of C. albicans Z-VAD-FMK molecular weight to adhere to polystyrene (Rodier Maraviroc et al., 2003). This information supports our results, as specific IgG isotypic recognition was confirmed for the complex of the CR3-RP antigen and polyclonal anti-CR3-RP antibody by immunocytometry. Moreover, the higher specificity of our anti-CR3-RP can be predicted because the sequence of the CR3-RP fragment used to immunize the rabbit is known (Bujdákováet al., 2008). The higher specificity was also evidence of a lower dilution of OKM1 mAb (1 : 10; a higher dilution was not possible because of low activity) used in all experiments in comparison with polyclonal anti-CR3-RP antibody (1 : 100). The reduction in the adherence capability of C. albicans due to blocking the CR3-RP surface antigen can effectively decrease biofilm formation. Additionally, despite the fact that adhesion

takes a relatively short time, changes in the capability of C. albicans to interact with a surface affected the formation of the biofilm, which was not able to revitalize in the later biofilm stages, resulting in a decrease in final biofilm fitness. This work was supported by financial contributions from EU project CanTrain MRTN-CT-2004-512481 as well as MVTS 6RP/MRTN-CT-2004-512481 and VEGA 1/0396/10 from the Clomifene Slovak Ministry of Education. “
“Citation Kraus TA, Sperling RS, Engel SM, Lo Y, Kellerman L, Singh T, Loubeau M, Ge Y, Garrido JL, Rodríguez-García M, Moran TM. Peripheral blood cytokine profiling during pregnancy and post-partum periods. Am J Reprod Immunol 2010; 64: 411–426 Problem  Pregnancy requires that the maternal immune system adapt to prevent rejection of the fetal semi-allograft. This immunologic adaptation may contribute to pregnancy-related alterations in disease susceptibility and severity of infections from viral pathogens such as influenza virus. Method of Study  As part of a larger study investigating the maternal systemic immune response during pregnancy, peripheral blood was collected three times during pregnancy and twice post-partum to measure serum levels of 23 cytokines, chemokines, and growth factors.

3b) because of the abundance of mDCs within the same gate. An alternative ex vivo approach to induce NK cell activation and cytokine production is through co-culture with NK-sensitive target cells. First, using a flow cytometry-based killing assay, we confirmed the ability of unstimulated,

as well as IL-2-stimulated and IL-15-stimulated, macaque PBMCs to kill the MHC-devoid human cell line 721.221. As shown in Fig. 4(a), treatment with both IL-2 and IL-15 significantly increased the killing capacity compared with non-stimulated buy Cabozantinib PBMCs at different E : T ratios ranging from 40 : 1 to 5 : 1 (P < 0·001 for both cytokines at a 40 : 1 E : T ratio). Second, using the 721.221-based NK cell activation assay, we analysed the effect of E : T cell co-culture on the activation status of CD8α− and CD8α+ NK cells. To accomplish this, IL-2-treated and IL-15-treated PBMCs were cultured at a 5 : 1 E : T ratio with 721.221 cells for 6 hr before mAb staining and flow cytometry analysis (which included CD11c and HLA-DR to gate out mDCs in both NK cell subpopulations). Co-culture of IL-15-treated PBMCs with 721.221 cells induced the expression of CD69, CD107a and IFN-γ on the surface of CD8α+ NK cells. CD8α− NK cells

up-regulated the expression of CD69 and IFN-γ (Fig. 4b,c), while showing a modest trend for up-regulation of CD107a (Fig. 4d). Having found that CD8α− NK cells express some NK cell lineage

markers and become activated upon cytokine and target cell stimulation, we directly investigated the cytokine-producing click here and cytolytic potential of the entire population of CD8α− NK cells which included the mDCs. CD8α− and CD8α+ NK cells were sorted by FACS using fluorochrome-conjugated anti-CD3, anti-CD20 and anti-CD8 mAbs. The CD8α− NK cells were enriched to a 95% pure population. CD8α+ NK cells (97% pure) and CD8− CD20+ B cells (97% pure) were used as positive and negative controls, respectively (Fig. 5a). As described above, only approximately 35% of enriched CD8α− NK cells were negative for DOK2 CD11c and HLA-DR expression. However, further purification of CD8α− NK cells to exclude mDCs was not possible because of limitations on the amount of blood allowed to be drawn from individual rhesus macaques. Because contaminating mDCs would not interfere in the functional assays, we proceeded to characterize the activities of NK cells present in the highly enriched CD8α− NK cell population. As CD8α− NK cells only minimally up-regulated the expression of IFN-γ (Fig. 4c) but did not up-regulate expression of TNF-α significantly (Fig. 3c), we further investigated expression of these and other cytokines by evaluating mRNA transcription of both genes in the enriched cell populations after 5 hr of IL-2 plus IL-15 treatment.

The resulting preparations were consistently >90% CD19+CCR6+. After separation cells were resuspended in PBS (Sigma), supplemented with 0.2% BSA and 0.01% sodium azide, and incubated with fluorochrome-conjugated mAb and isotype-matched negative controls (DakoCytomation, Milan, Italy) after blocking nonspecific sites with rabbit IgG (Sigma) for 30 min at 4°C. Nutlin-3a purchase The following PE-conjugated mAb were used: anti-CD1a, anti-CCR6 (both from R&D Systems), anti-langerin

(BD Biosciences). FACS analysis was performed with an FACSCalibur and CELLQuest software (BD Biosciences). Cells were gated according to their light-scatter properties to exclude cell debris and contaminating lymphocytes. Migration measurements were made in duplicate using a transwell system (24-well plates; 5.0 μm pore buy Ibrutinib sizes; Costar, Corning, NY, USA). A total of 600 μL of supernatant from LacZ and IFI16 infected HUVEC preincubated or not in the presence of anti-CCL4, anti-CCL5 and anti-CCL20 mAb for 30 min at room temperature were added to the lower chamber. A total of either 1.5×105 L-DC or B cells in 100 μL were added to the upper chamber and incubated at 37°C for 2 h. Cells that migrated into the lower chamber were harvested and counted by flow cytometry acquiring events for a fixed time of 30 s. The range of the control titration curves obtained by testing increasing concentrations of cells. The results are expressed

as the mean number of migrated cells±SEM 28. Unpaired Student’s t-tests were used to determine whether the differences in migration were statistically significant. Statistical analyses were performed using GraphPad Prism version 5.00 for Windows (GraphPad Software, San Diego, CA,

USA, www.graphpad.com). This work was supported by grants from Regione Piemonte (‘Ricerca Sanitaria Finalizzata’ 2008, 2008bis and 2009 to M. D. A., M. M., M. G. and S. L.), Italian Ministry for University MIUR (PRIN 2008 to M. G. and S. L., and FIRB – Futuro in Ricerca 2008 to M. D. A.), Fondazione CRT (“Progetto Alfieri” to S. L.). P. C. is supported by a fellowship from Fondazione Italiana per la Ricerca sul Cancro. PBMC, B cells and DC were derived from the peripheral blood of healthy donors from the Blood Bank under an Institutional Review Board-approved Silibinin protocol. Conflict of interest: The authors declare no financial or commercial conflict of interest. “
“Neuro-Behçet’s disease (NBD) is a serious complication of Behçet’s disease. Generally, NBD patients with a chronic course are refractory to immunosuppressive treatment, resulting in the deterioration of personality. In this study, levels of B cell-activating factor belonging to the TNF family (BAFF) were measured in the cerebrospinal fluid (CSF) from 18 patients with NBD, 27 patients with epidemic aseptic meningitis (AM), 24 patients with multiple sclerosis (MS) and 34 healthy controls.