Most (40 spots) of

altered protein spots had pI of 4·5–7 and equal numbers of proteins were upregulated or downregulated (Figure 1). In addition, nine of the altered proteins had pI of 6·7–10, with an increase in the expression levels of five proteins and a decrease in those of four proteins as a result AG 14699 of O. viverrini infection (Figure 2). When these protein spots were subjected to MALDI-TOF analysis, the distribution of the altered proteins according to their functions is summarized in Table 3. Proteins involved in fatty acid cycle, metabolism, blood volume maintenance, energy and transcription decreased in O. viverrini-infected hamsters. The decrease in proteins related to fatty acid cycle and metabolism is supported by reports of deposition of lipid droplets and glycogen in the liver cells of O. viverrini-infected hamster (21), and of decreased cholesterol synthesis in opisthorchiasis patients (22), leading to impaired absorption of fats and carbohydrates by the small intestine (23). The decreased proteins were related to blood volume maintenance such as albumin precursor, leading to decreased level of total protein and albumin in serum in opisthorchiasis patients (13). On the

other hand, several proteins upregulated by O. viverrini infection included those related to fatty acid cycle (2·2-fold), translation (1·5-fold), metabolism (1·5- to 2·9-fold), signal transduction (1·5-fold), cell structure (actin) (1·9- to 3·3-fold), DNA replication Decitabine manufacturer and repair (recR) (3·4-fold), energy (3·9-fold) and antioxidative activity (Prdx6) (2·7-fold). The increased expression of structural components is consistent with the accumulation of periductal fibrosis induced by O. viverrini infection (19,24), but this is the first report of an increased actin

expression. Moreover, we demonstrated that actin isoform 2 increased 1·9-fold Palbociclib mw during infection. This result is supported by a finding that the expression patterns of different actin isoforms or of modified actins have been reported during parasitic infection (17). It has been previously demonstrated that oxidative and nitrative DNA damage participates in inflammation-mediated carcinogenesis in hamsters infected with O. viverrini (10). Thus, the expression of recR may contribute to the repair of damaged DNA and suppression of carcinogenesis. RecR may also participate in the repair of cell injury (viz. epithelial bile duct cell, liver cell and inflammatory cell) and in the suppression of cell division mediated by free radicals and inflammation-related cytokines during chronic inflammation (18,25,26). Prdx6 is a cytosolic member of the family of antioxidant proteins, Prdxs, and its expression is upregulated in response to cell growth and oxidative stress (12,27). In this study, we detected increased expression of Prdx6 (spot No. 20) in O. viverrini-infected hamsters using 2DE. Expression of Prdx6 was also detected by 2DE and immunoblot analysis (Figure 3a).

Recent work revealed that Dar is an enlargement of rectal epithelial cells K/K′, F, U and B [42]. Genetic analysis has shown that host-encoded sugar transporters and acyltransferases are required for microbial attachment to the anus and induction of the Dar phenotype [43]. In addition, the swelling response requires an extracellular-regulated kinase (ERK) signalling pathway, as does inflammation in mammalian cells [43,44]. These results provided a cellular explanation

for the Dar phenotype, and revealed for the first time a role for the rectal epithelium in the host response to infection. Interestingly, forward genetic screens for mutants defective in the swelling response to M. nematophilum identified the HOX gene egl-5. EGL-5 is required in the rectal epithelial cells for the transcription of the ERK homologous Selleckchem LDE225 gene mpk-1[45]. S. aureus infection also causes a swelling response in the anal region, although in this case the involvement

of the rectal epithelial cells is still conjecture. Despite having a defective transcriptional host response to S. aureus infection, egl-5 mutants are not defective in the swelling response to S. aureus[9]. In contrast, the β-catenin gene bar-1, PS-341 price which acts upstream of egl-5 during Wnt signal transduction, is required both for the swelling response and the transcriptional host response to S. aureus infection (J. E. Irazoqui and F. M. Ausubel, unpublished). Thus, even if the same cells were involved in the responses to M. nematophilum PRKD3 and S. aureus, the signalling pathways required for cell swelling are distinct. Further work is required to identify the components of each different pathway. Several genes induced during infection with S. aureus or P. aeruginosa are expressed in the rectal gland, a group of cells directly apposed to the rectum that are thought to secrete molecules into the rectal lumen [9,10] (J. E. Irazoqui and F. M. Ausubel, unpublished). This is consistent with a potential role for rectal gland cells in secretion of immune defence molecules into the rectal lumen. Further study is required to test this hypothesis. Although it is clear that C.

elegans lacks a bona fide circulatory system with sessile professional phagocytes, C. elegans does have phagocytes that reside in its body cavity, the pseudocoelom. Three pairs of static coelomocytes are located in ventral anterior, ventral posterior and dorsal posterior locations, where they constitutively endocytose pseudocoelomic fluid [46]. The coelomocytes have been proposed to function in immune surveillance, although direct experimental evidence is lacking [46]. The collagenous cuticle that encases the C. elegans body provides a highly impermeable physical barrier with the environment. However, some bacteria have learned to exploit this surface to their advantage. Forward genetic analysis has identified components of the cuticle required for M. nematophilum binding and for Yersinia biofilm formation [47,48].

28 Chagnac et al.29 demonstrated that renal hyperperfusion and hyperfiltration in severe obesity and hyperfiltration injuries can lead to the final pathway of glomerulosclerosis MK0683 price especially when the size of functioning nephron mass is substantially reduced. As a result, obesity might have more adverse effects in renal transplant recipients. A major limitation in our study is the relatively small sample size. Moreover, the underweight patients (BMI <18.5) in our study were not analyzed separately because of the limited number of patients. More patients should be recruited in order to see if Asian renal transplant recipients

with low BMI values have a higher mortality when compared with recipients with normal BMI values. Furthermore, lack of data for those with primary non-functioning kidneys was another limitation in this study because obese patients tend to experience more surgical problems which may result in early technically-caused graft loss. Finally, our obese patients were older and had a higher incidence of DM, so survival analysis could still

be biased because both were independent predictors of graft outcome. However, with the use BVD-523 ic50 of a multivariate model of factors associated with graft failure over time, we demonstrated that obesity was associated with decreased long-term graft survival independent of confounding factors such as DM and age. In conclusion, our study demonstrated that obesity was significantly associated with poor renal graft function and decreased patient and graft survival in Asian renal transplant recipients. In addition, overweight was associated with a lower estimated GFR. However, no significant difference in patient and graft survival could be demonstrated between the overweight group and the normal group. Further studies are required to

validate the optimal target BMI in our renal transplant recipients. Moreover, we also showed that obesity, older age, Telomerase presence of pre-transplant DM and acute rejection were all independent risk factors for graft failure in our patients. “
“Aim:  Diabetic patients are at higher risk of failure to recover after acute kidney injury, however, the mechanism and therapeutic strategies remain unclear. Erythropoietin is cytoprotective in a variety of non-haematopoietic cells. The aim of the present study was to clarify the mechanism of diabetes-related acceleration of renal damage after ischaemia–reperfusion injury and to examine the therapeutic potential of asialoerythropoietin, a non-haematopoietic erythropoietin derivative, against ischaemia–reperfusion-induced acute kidney injury in diabetic mice. Methods:  C57BL/6J mice with and without streptozotocin-induced diabetes were subjected to 30 min unilateral renal ischaemia–reperfusion injury at 1 week after induction of diabetes.

Indeed, the CD27 molecule, which is expressed on the majority of Vγ9Vδ2+ peripheral selleck chemicals llc blood lymphocytes 5, provides enhanced proliferative capacity in vitro when engaged with its natural ligand CD70. Furthermore, a soluble recombinant CD70 construct, which the authors use in lieu of the natural ligand, induces calcium signals as well as increased transcription of cell cycle-associated Cyclin D2 and anti-apoptotic Bcl2a1 genes 8. In experiments that either abrogate or restore CD27-CD70 interactions involving Vγ9Vδ2+ cells, their proliferation, cytokine production and survival are altered correspondingly 8. In particular, CD27 costimulation

of Vγ9Vδ2+ PBLs upon stimulation via the TCR with phosphoantigens 10, selectively enhances the expansion of CD27+ Vγ9Vδ2+ cells with a Th1 functional bias 8. These findings establish that CD27 can act as a coreceptor in synergy with the human γδ TCR, and suggest that CD27 engagement enables functional differentiation, both quite similar to the observations made in mice. As pointed out by the authors 8, this could be very important when trying to manipulate γδ T-cell functions for clinical immunotherapy. Certainly, the intriguing observation that JQ1 datasheet CD27 expression is linked to

functional differentiation of both murine and human γδ T cells deserves further consideration. Since engagement of CD27 leads to Th1-biased cytokine production 6, 8, CD27 seems to play a role at the end of this process; however, the type of γδ T cell that expresses this receptor might be also important. Studies in mice have suggested a correlation between γδ T-cell function and the expression of TCR-V genes or certain invariant TCRs, initially because γδ T cells expressing distinct TCRs segregate into different tissues and organs, and subsequently because adoptively transferred purified γδ T cells expressing different TCR-Vs exerted distinct effects

in various models of disease 11–14. Similarly, ex vivo and in vitro studies with TCR-V-defined human γδ T cells indicate such functional differences 15. Despite HSP90 these correlations, it is not clear whether TCR specificity provides a basis for the functional differences. Instead, as γδ T cells expressing different TCRs develop separately in ontogeny, perhaps other functionally relevant receptors follow suit. Thus, Vγ1+ γδ T cells in mice often express NK1.1 14, which is consistent with an NKT-like functional profile, and Vγ4+ cells more frequently express CD8αβ 14 along with cytolytic activity. When Ribot and colleagues 6 examined murine CD27+ γδ T cells in the spleen and lymph nodes, after in vitro culture and stimulation with PMA/ionomycin, the majority (71%) expressed Vγ1 whereas a minority (15%) expressed Vγ4.

The core regions acted as focal points of subsequent research, mainly

because they were more soluble than their full-length counterparts. Using surface plasmon resonance and in vivo one-hybrid experiments, it was shown that the see more N-terminus of cRAG1 (amino acids 384–460) harbours the nonamer binding region.[28] The heptamer recognition region of RAGs still remains obscure. The DDE motif (a triad of three acidic amino acids: D600, D708 and E962) of RAG1 forms the catalytic centre of the RAG1/RAG2 complex,[64-66] which plays a role in chelating the two divalent metal ions essential for catalysis.[67] The N-terminal non-core region (amino acids 1–383) contains a RING domain fold, which exhibits ubiquitin ligase activity.[68] Studies by Rodgers’s group[63] using limited proteolysis showed that murine cRAG1 is composed of topologically independent domains that can function individually. These include the N-terminal, the central and the C-terminal domains. The central domain has the heptamer binding site, RAG2 binding site and zinc

finger motif. The C-terminal domain has the dimerization region and binds DNA co-operatively. Murine cRAG1 was successfully expressed in Escherichia coli as a fusion protein with Maltose binding protein (MBP) tag with high yield and solubility and was active when combined with cRAG2 expressed in human embryonic kidney cell line.[69] However, there is no report of successful bacterial expression of RAG2. Murine ‘core RAG2’ consists of amino MLN2238 acids 1–383 out of the total 527. The molecular function of core RAG2 remains elusive. RAG2 consists of an N-terminal 6-bladed beta-propeller domain and a C-terminal plant homeo domain (PHD).[70, 71] The PHD is a motif characteristic of chromatin remodelling proteins.[72] It has been predicted to facilitate the ordered Grape seed extract rearrangement of IgH chains and the binding of core histone proteins.[72-74] The C-terminus of RAG2 contains a threonine residue (T490)

that acts as a target of Chk2 kinase.[75] Phosphorylation of this amino acid regulates the proteosomal degradation of RAG2 at the G1/S transition of the cell cycle.[76] This regulatory mechanism ensures that RAG2 is degraded in a cell-cycle-dependent manner preventing RAG-induced DNA breaks during replication. Biochemical analysis of recombinant RAG2 has identified several basic residue mutants defective in catalysis. Accordingly, Schatz’s group[77] has proposed a model for the interaction of RAG2 with DNA in which the amino acids K119 and K283 directly contact DNA. It was shown that the PHD finger specifically recognizes histone 3 trimethylated at lysine 4 (H3K4me3).[78] The H3K4me3 increases the catalytic turnover number (Kcat) of RAGs as well as tethering it to DNA.

1(a), LTC4 increased in a dose-dependent manner, the expression of MHC class II on immature DCs was more significant at 10−8 m, so the trials were conducted using this concentration. Then, considering that LTC4 is released during inflammatory responses,17,30 we studied the effect of LTC4 (10−8 m) on the phenotype of immature DCs and LPS-stimulated DCs. Interestingly, after selleck kinase inhibitor 18 hr of culture, LTC4 strongly inhibited the expression of CD86 and CD40 molecules (Fig. 1b,c,f) when DCs were activated with 1 μg/ml LPS, whereas the lipid mediator

had no effect on immature DCs. However, in the case of the class II molecules, LTC4 had antagonistic effects depending on the activation status of DCs, increasing its expression in immature DCs and inhibiting in LPS-treated DCs (Fig. 1d,f). As shown in Fig. 1(g), although MHC class II decreased its expression in LPS-activated DCs, LTC4 had the ability to prime T lymphocytes, because it induced a low but significant increase selleck screening library in the allostimulatory response mediated by activated DCs. This effect was also observed in immature DCs, which correlates with the increased expression of class II molecules by LTC4. Immature DCs are specialized to

sense the microenvironment and when stress or infection are detected they incorporate the antigen through phagocytosis or endocytosis.28,29,31,32 We aimed to determine whether LTC4 was able to affect the antigen uptake of immature and activated DCs. To this end, cells were treated or not with LPS (1 μg/ml) for 30 min at 37°, then DCs were incubated without or with 10−8 m LTC4 for 30 min at 37°. Finally, cells were washed and incubated in the presence of Zy (10 particles/DC) coupled to FITC for 30 min at room temperature or DX-FITC (100 μg/ml) for 40 min at 37°. The phagocytosis controls were supplied by DCs treated with cytochalasin B, a disruptor of actin microfilaments, 33 previous to their incubation with Zy-FITC. For DX endocytosis, the control of reaction was provided by DCs incubated with the antigen at 4°, because this is a temperature-dependent phenomenon. In

addition, we analysed the uptake of HRP. For this, after treatment with LTC4 (0·01 μm) of both DCs and LPS-stimulated DCs, these were cultured with 150 μg/ml HRP for 40 min at 37°. Subsequently, cells were washed Endonuclease several times with cold PBS and permeabilized by addition of 0·5% Triton X-100 in PBS for 30 min at room temperature. The control was provided by DCs treated with HRP but not permeabilized. Finally, the enzymatic activity was measured in supernatants of reaction by addition of the substrate [alpha-phenylendiamine (OPD)] and read at 492 nm. In Fig. 2(a), we demonstrated that LTC4 increased the phagocytosis of Zy-FITC by immature DCs but had no effect in LPS-activated DCs. In contrast, as shown in Fig. 2(b,c), uptake of DX and HRP was increased by LTC4 in both immature and LPS-stimulated DCs.

An additional ad hoc meta-analysis was performed on studies that reported a complete MBL2 genotypic profile inclusive of promoter polymorphisms. Although only a minority of

studies reported such data, this group was chosen as such genotype profiles are associated considerably more strongly with MBL serum levels than structural genotypes alone. Using this subset, patients and controls were reanalysed based on the frequency of high or low MBL-producing genotype. O/O and XA/O were considered low MBL-producing genotypes in this analysis, with other genotypes considered to be high MBL-producing. This analysis, shown in Fig. 3, did not demonstrate a significant effect of MBL2 genotype on likelihood of pulmonary TB infection

[25,28,31,33], with results influenced significantly by a single outlying study. Genotypes in HIV-positive patients.  Two studies [31,33] contained sufficient data to allow comparison of MBL2 wild-type versus MBL2 MG-132 concentration variant compound heterozygote genotype frequency in HIV-positive patients with and without tuberculosis infection versus healthy control. These studies included a total of 173 cases and 393 controls, and summary data are presented in Table 2. The two studies analysed conflict directly, with one Selleck NVP-AUY922 suggesting a protective effect of wild-type MBL2 genotypes and the other suggesting an increased susceptibility to TB infection. Neither study achieved statistical significance independently. When considered together, these results do not show a significant association between deficiency-associated MBL2 genotypes and TB susceptibility (OR 1·2, 95% CI 0·54–2·82). Serum MBL levels in HIV-negative patients.  Eight studies reported collection of serum MBL levels from at least some

subjects [19,20,23,27,28,33–35]. One study was excluded because it reported MBL levels in subjects with TB but not controls [28]. One study presented MBL levels only according to subject genotype, and the data did not permit overall comparison of subjects and controls [23]. One study was available only in abstract form in English and did not contain sufficient detail for inclusion [20]. One study contained data only on HIV-positive subjects [33]. In total, four studies contained sufficient data to allow comparison of serum MBL levels Methane monooxygenase in HIV-negative patients with and without tuberculosis [19,27,33–35]. The included studies contained a total of 341 patients with active tuberculosis and 349 controls. Three of the studies reported that serum was collected for MBL sampling prior to or shortly after the introduction of anti-TB therapy [19,27,35], while in the remaining study timing of sample collection was not reported [34]. One study also reported sampling an additional group of patients after completion of therapy [27]. In one study, MBL levels were not available in the published text, but were kindly provided for inclusion ([19]; P. Garred, personal communication).

In most behavioral experiments, eye gaze and head orientation have been used simultaneously to indicate a person’s focus of visual attention (Hoehl et al., 2009). However, it has been a matter of debate to what extent, if at all, young infants rely on information from the eyes instead of head orientation alone. For instance, Corkum and Moore (1995) reported that 12-month-olds follow someone’s head turn to the side even if the person maintains eye contact with them. In a later experiment, the authors found that only 18-month-olds, but not younger infants, followed an experimenter’s isolated

eye movements (Moore & Corkum, 1998). A more recent study showed that eye gaze influences 12-month-olds’ attention allocation to the ceiling more than head orientation (Tomasello, Hare, Lehmann, & Call, 2007). Correspondingly, Meltzoff and Brooks (2007) reported MK-1775 datasheet that 10-

to 11-month-olds follow someone’s head turn to the side when the person’s eyes are open, but refrain from doing so when her eyes are closed, indicating an understanding of “looking” as involving open eyes. However, younger infants in these experiments followed head turns even when the experimenter’s eyes were closed (Meltzoff & Brooks, check details 2007). Thus, although the age at which the status of the eyes becomes relevant for infants’ following of others’ attention focus varies in different studies between 10 and 18 months, it is quite unequivocal that younger infants are more

affected by head direction and hardly seem to take into account the eyes at all. In contrast to these studies on overt gaze following, research using attention cueing paradigms showed that 3-month-olds (Hood, Willen, & Driver, DOK2 1998) and even newborns (Farroni, Massaccesi, Pividori, & Johnson, 2004) allocate attention in the direction of eye gaze cues. These studies differ from the aforementioned gaze following studies in that they involve computer presentations instead of live actors and shorter distances between face and target. It has been suggested that gaze cueing effects in very young infants rely on rather automatic processes to be distinguished from more deliberate gaze following and joint attention in live studies with older infants (Moore & Corkum, 1998). However, eye gaze seems to serve a function in directing young infants’ attention and thereby affecting their processing of objects (Hoehl et al., 2009). Using event-related potentials (ERPs), Reid, Striano, Kaufman, and Johnson (2004) presented 4-month-olds with full frontal view faces directing gaze toward or away from peripheral objects. When objects were subsequently presented again, those objects that were not cued by the person’s eye gaze elicited a more pronounced brain response. On the behavioral level, uncued objects also received more of 4-month-olds’ attention than cued objects in a visual preference task (Reid & Striano, 2005).

1A–D). NK1.1+ αβTCR+ T cells from HMNC consist of CD4+ and CD4− cells (Supporting Information Fig. 1). When OT-II CD4+ T cells were stimulated in the presence of CD4+ or CD4− NKT cells, CD4+ NKT cells effectively inhibited Th1 and Th17 differentiation of CD4+ T cells, but CD4− NKT cells showed rather weak inhibitory effects (Supporting Information Fig. 3). We next evaluated the mechanism underlying the invariant NKT cell-mediated suppression of IL-17 production. NKT cells secrete large amounts of Th1 and Th2 cytokines

following stimulation through their TCR 18, 19, and cytokines produced by activated NKT cells could influence Th differentiation. To evaluate the impact of cytokines from NKT cells, NK1.1+-depleted OT-II lymph node cells were co-cultured with FACS-purified NKT cells from WT, IL-4−/−, IL-10−/−, or find more IFN-γ−/− mice and stimulated

with OVA peptide in the presence of Th17-promoting cytokines. NKT cells from both the WT and the cytokine-deficient mice displayed inhibitory effects on Th17 differentiation in co-culture experiments. Although the NKT cells from WT mice demonstrated the maximal inhibitory capacity (**p<0.00005 versus control without NKT cells) (Fig. 1E and F), cells from IL-4−/−, IL-10−/−, or IFN-γ−/− mice also demonstrated significant inhibition of Th17 differentiation (*p<0.0005 versus control without NKT cells) (Fig. 1E and F). The observation that specific cytokine-deficient NKT cells sufficiently suppressed Th17 differentiation suggests that factors other than the cytokines produced by NKT cells Selleck INCB024360 may inhibit the differentiation of CD4+ T cells into Th17 cells and/or that Th17-promoting conditions may alter the cytokine production of the NKT cells. Consequently, we analyzed the cytokine profiles produced when NKT cells were activated in the presence of IL-6 and TGF-β. Compared

with the Th0 culture conditions, IFN-γ production was markedly reduced (Fig. 2A). This result suggests that IFN-γ, a well-known inhibitor of IL-17+ cell production, produced from activated NKT cells was not the major influence on Th17 differentiation under Th17-promoting conditions. The production Verteporfin in vitro of IL-4, IL-10, and IL-17 from activated NKT cells, however, was not changed by the presence of IL-6 and TGF-β and increased in proportion to the α-GalCer dose (Fig. 2A). To evaluate whether the Th17-inhibiting effect of NKT cells was due to the increased production of cytokines other than IFN-γ, we added serial dilutions of α-GalCer during the OT-II cell activation under Th17-promoting conditions. Even following stimulation with the lowest concentration of α-GalCer used (0.16 ng/mL), the NKT cells (3.5×104 cells/well) successfully inhibited Th17 differentiation, effecting a 75% reduction in the number of IL-17-producing CD4+ T cells (Fig. 2B). Next, we titrated the number of NKT cells added to the co-culture experiments. The number of added NKT cells paralleled the degree of Th17 suppression (Fig. 2C).

In our ELISAs, anti-mouse IgG antibodies were buy Ceritinib used as the secondary antibodies. It was reported previously that anti-mouse IgG antibodies react to the IgG of various species of rodent, including Apodemus spp. and Myodes spp., which are the main natural mammalian hosts for the TBE virus (32). The reactivity to the IgG of Myodes rufocanus is relatively low when compared to that to the IgG of Mus musculus (35.9%). The three false-negative samples in SP-ELISA were from M. rufocanus. It is possible that the lower reactivity might cause the false-negative results in the samples of M. rufocanus; however, because

the most of the positive samples of M. rufocanus were detected, including

the samples from the field survey, in a TBE virus-endemic area, the anti-mouse IgG antibodies in our ELISA are useful in large-scale epizootiological survey in various species of wild selleck chemicals rodents. The EdIII-ELISA and SP-ELISA were applied to the epizootiological survey of wild rodents in Khavarovsk, Russia, in which many TBE patients are reported annually (24). Both ELISAs could detect TBE virus-infected rodents, which were also confirmed by the neutralization test. Therefore, the ELISAs are suitable for screening to detect TBE virus-infected rodents by investigating a number of rodent samples, and they are useful for specifying a TBE virus-endemic area. In summary, we developed the ELISAs using domain III of the E proteins and the SPs as the antigens. The ELISAs had high sensitivity and specificity, and it was shown that SP antigens had higher detection accuracy than below domain III antigens. The ELISAs were also shown to be applied to the epizootiological research in TBE virus-endemic area. This is the first study to show the serological diagnosis of wild rodents using recombinant antigens and the ELISAs can be safe and useful in the detection of TBE virus-infected wild rodents in epizootiological research. This work was supported by Grants-in-Aid for Scientific Research (22780268) and the global COE program from

the Ministry of Education, Science, Sports and Culture of Japan, and Health Sciences Grants for Research on Emerging and Re-emerging Infectious Disease from the Ministry of Health, Labor and Welfare of Japan. “
“Aryl hydrocarbon receptor (AhR) is well known for mediating the toxic effects of dioxin-containing pollutants, but has also been shown to be involved in the natural regulation of the immune response. In this study, we investigated the effect of AhR activation by its endogenous ligands 6-formylindolo[3,2-b]carbazole (FICZ) and 2-(1′H-indole-3′-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) on the differentiation, maturation and function of monocyte-derived DCs in Behçet’s disease (BD) patients.