5 months. Fourteen surveillance cultures demonstrated

21 isolates of Aeromonas species, 71.4% of which were PFT�� molecular weight ciprofloxacin susceptible. All isolates were sulfamethoxazole-trimethoprim (SXT) susceptible. The prophylactic antibiotic regimen of choice for leech therapy at our institution is SXT, with culture of tank water to refine antimicrobial choice if necessary. This study demonstrates the importance of regular surveillance to detect resistant Aeromonas species in medical leeches; however optimal practice has not been established. © 2013 Wiley Periodicals, Inc. Microsurgery, 2013. “
“The reconstruction of nasal defects together with nasal lining, skeletal support, and skin loss constitutes difficulty to plastic surgeons. We present a single-stage reconstruction of the defect formed on the nasal tip, columella, septum, and upper lip after tumor excision by performing free temporoparietal fascial flap, costal cartilage, and skin graft. In this case, cartilage support was created by the graft taken from costal cartilage, and free temporoparietal fascial flap was wrapped around this cartilage PF-6463922 in vitro scaffold. Skin graft taken from scalp was placed on the skin surface, and skin graft taken from the thigh was placed on the mucosal surface. Vascular anastomoses were performed on the labial artery and the concomitant

vein. In consequence of this operation, a nasal reconstruction with acceptable esthetic and functional results was Glutamate dehydrogenase provided in a complex nasal defect. Internal lining, skin, and cartilage structures were replaced in one single stage and with single flap and graft. © 2012 Wiley Periodicals, Inc. Microsurgery, 2013. “
“White light spectroscopy non-invasively measures hemoglobin saturation at the capillary level rendering an end-organ measurement of perfusion. We hypothesized this technology could be used after microvascular surgery to allow for early detection of ischemia and thrombosis. The Spectros T-Stat monitoring device, which utilizes white light spectroscopy, was compared with traditional flap

monitoring techniques including pencil Doppler and clinical exam. Data were prospectively collected and analyzed. Results from 31 flaps revealed a normal capillary hemoglobin saturation of 40–75% with increase in saturation during the early postoperative period. One flap required return to the operating room 12 hours after microvascular anastomosis. The T-stat system recorded an acute decrease in saturation from ∼50% to less than 30% 50 min prior to identification by clinical exam. Prompt treatment resulted in flap salvage. The Spectros T-Stat monitor may be a useful adjunct for free flap monitoring providing continuous, accurate perfusion assessment postoperatively. © 2012 Wiley Periodicals, Inc. Microsurgery, 2013.

is their dissemination through blood vessels until they reach target organs (mainly

lung and gut). There are no direct data on the role of Strongyloides spp. infection on angiogenesis. However, both indirect evidence in experimental model (3), and human hyperinfection (demonstration of vascular anomalies by arteriography or endoscopy) (5,6) suggest the involvement of angiogenic factors in the pathogenesis of this infection. Angiogenesis is the process of new blood vessel formation from pre-existing ones, plays a key role in various physiological and pathological conditions, including embryonic development, wound repair, tumour growth and inflammation (7). Angiogenesis is initiated by vasodilatation and an increased permeability being regulated by a delicate balance of pro and anti-angiogenic factors. Amongst angiogenic factors, vascular endothelial growth factor

(VEGF)/vascular Ku-0059436 mw permeability factor and fibroblast growth factor-2 (FGF-2) are the best characterized positive regulators. In particular, VEGF has distinct specificity Luminespib molecular weight for vascular endothelial cells (8). The biological actions of VEGF include stimulation of endothelial cell proliferation, migration, differentiation, tube formation, vascular permeability and maintenance of vascular integrity (9). FGF2 is less specific for endothelial cell proliferation, but is a potent angiogenic factor in vitro and in vivo (10). Moreover, many endogenous inhibitors of angiogenesis have been described, endostatin (C-terminal fragment of collagen XVIII) and angiostatin being the best characterized (11). Although the precise mechanism for the antiangiogenic effect of endostatin is not well known, this molecule can block endothelial cell proliferation, survival and migration through blocking VEGFR2 signalling and other mechanisms (12). The aim of this study was

Isotretinoin to evaluate the role of angiogenic and angiostatic factors in the pathogenesis of experimental strongyloidiasis. We used two complimentary approaches: (i) an in vivo model of infection by S. venezuelensis in CD1 mice was used for the evaluation of the effect of endostatin on the parasitic infection and for the mechanisms involved in the reduction of parasite burden, (ii) an in vitro study of the antigens responsible for stimulation of angiogenic factors from alveolar macrophages and the mechanisms involved in their production. Male Wistar rats and female CD1 mice were purchased from Charles River Laboratories, Barcelona, Spain. All experiments of this work comply with current European Union law on animal experimentation. All infected and control animal strains were maintained under standard laboratory conditions in the animal experimentation facilities of the Salamanca University.

However, insulin receptors and insulin signaling are not exclusively restricted to skeletal muscle, but can also be Selleckchem Compound Library observed in vascular cells. Insulin directly targets the endothelial cell where it stimulates NO release from the vascular endothelium in a PI3K-dependent manner that involves the Akt-mediated phosphorylation of eNOS, which leads to vasodilatation [84]. Alternatively, insulin also activates the mitogen-activated protein kinase pathway in endothelial cells, which enhances the generation of the vasoconstrictor ET-1 via ERK1/2 signaling [84,96]. In healthy subjects,

the vasodilatory signal predominates, but if signaling from the insulin receptor to eNOS is inhibited pharmacologically or downregulated by insulin resistance, this can lead to impaired

insulin-mediated vasodilatation or even insulin-stimulated vasoconstriction. In this manner, vascular insulin resistance may contribute to the development of hypertension and impaired overall insulin-stimulated buy BGB324 glucose uptake [64,73,97]. In obese rats, the insulin-signaling pathways are selectively impaired: insulin-mediated activation of PI3-kinase, Akt and eNOS is impaired, but insulin-mediated activation of ERK1/2 is intact [29,51]. Recently, it has been demonstrated that impaired insulin signaling in endothelial cells, due to reduced IRS2 expression and insulin-induced eNOS phosphorylation, caused attenuation of insulin-induced capillary recruitment and insulin delivery, which in turn reduced glucose uptake by skeletal muscle [64]. Moreover, restoration of insulin-induced eNOS phosphorylation in endothelial cells completely reversed Cepharanthine the reduction in capillary recruitment and insulin delivery in

tissue-specific knockout mice lacking Irs2 in endothelial cells and fed a high-fat diet. As a result, glucose uptake by skeletal muscle was restored in these mice. These results show that insulin signaling in endothelial cells plays a pivotal role in the regulation of glucose uptake by skeletal muscle. Notably, during obesity induced by high fat feeding, inflammation and insulin resistance developed in the vasculature well before these responses were detected in the muscle, liver, or adipose tissue [61]. This observation suggests that the vasculature is more susceptible than other tissues to the deleterious effects of nutrient overload, and may play a pathophysiological role in inducing insulin resistance. The contribution of insulin signaling to the regulation of blood pressure in different states of insulin resistance is less unequivocal [108]. In healthy humans, insulin has also been shown to stimulate both ET-1 and NO at the level of the resistance vessels of forearm [11]. Moreover, obese, hypertensive humans show an insulin-induced vasoconstriction [37], as well as increased ET-1-dependent vasoconstrictor tone and decreased NO-dependent vasodilator tone at the level of the resistance arteries [10].

JT and MK performed pyrosequencing analysis. CM

and XM participated in the design of the study and helped draft the manuscript. RS helped with statistical analysis. All authors read and approved the final manuscript. This work was supported by grants from French Ministry of Research: Agence Nationale pour la Recherche (ANR) 2010-BLAN-1133 01 and by the Société Française de Rhumatologie (SFR): R. Belkhir CAL-101 clinical trial received a research bursary for 2009–2010. “
“We investigated the role of B cell lymphoma (BCL)-2-interacting mediator of cell death (Bim) for lymphocyte homeostasis in intestinal mucosa. Lymphocytes lacking Bim are refractory to apoptosis. Chronic colitis was induced in Bim-deficient mice (Bim–/–) with dextran sulphate sodium (DSS). Weight loss and colonoscopic score were increased significantly in Bim–/– mice compared to Y-27632 supplier wild-type mice. As Bim is induced for the killing of autoreactive cells we determined the role of Bim in the regulation of lymphocyte survival at mucosal sites. Upon chronic dextran sulphate sodium (DSS)-induced colitis, Bim–/– animals exhibited an increased infiltrate of lymphocytes into the mucosa compared to wild-type

mice. The number of autoreactive T cell receptor (TCR) Vβ8+ lymphocytes was significantly higher in Bim–/– mice compared to wild-type controls. Impaired removal of autoreactive lymphocytes in Bim–/– mice upon chronic DSS-induced colitis may therefore contribute to aggravated mucosal inflammation. Pro-survival B cell lymphoma (BCL)-2 interacts with pro-apoptotic BCL-2-interacting mediator of cell death (Bim). Bim is sequestered to microtubules [1], by which Bim can be separated from BCL-2. Upon apoptotic stimuli, such as ultraviolet (UV) irradiation and growth factor withdrawal, Bim translocates Baf-A1 supplier to BCL-2 and neutralizes its anti-apoptotic activity. This process does not require caspase activity, and therefore constitutes an initiating event in apoptosis signalling. Bim was suggested to have an increased

prevalence of phosphorylation sites. Bim is phosphorylated and targeted for degradation by the proteasome [2]. Inactivation of BCL-2 has been suggested to be the key to the ability of Bim to induce apoptosis. However, an alternative model argues that some forms of Bim can also bind directly to the other pro-apoptotic proteins Bax and Bak in order to initiate apoptosis [3]. Bax and Bak act by forming pores in the mitochondrial membrane, finally triggering apoptosis. Other BH3-only proteins, such as Bmf, Bad, Noxa and Puma, are considered to act as sensitizers which bind the pro-survival BCL-2 protein and thereby displace Bim from BCL-2 to promote cell death [4]. Bim transduces death signals not only after its release from the actin cytoskeleton, but also by activation of its transcription. Bim transcription is induced by transforming growth factor (TGF)-β-driven apoptosis in a number of cell types [5].

Some toxicity has not been recognized until recently and

by the Western world, rather than China. One of the representative samples is the emerging term ‘Chinese herbs nephropathy (CHN)’ since the 1990s, later renamed ‘aristolochic acid nephropathy (AAN)’, which has been reported after the introduction of Chinese herbs in a slimming regimen followed by young Belgian women.[3] It is now known Ferroptosis inhibitor that AAN has contributed to the very high incidence of end-stage renal disease (ESRD) in Taiwan[4] and about 80% of chronic tubular and interstitial nephritis in mainland China.[5] However, a case of an aristolochic acid containing herb Mutong induced acute renal failure has been reported as early as 1964

in a Chinese paper.[6] At least two more cases have been reported before Western scientists declared the discovery of CHN.[7, 8] If only these reports had been noticed and valued by the academic and Western world, AAN would have been discovered much earlier and the tremendous number of ESRD patients would have been saved. Andrographis paniculata (Burm. F) Nees, generally known as ‘king of bitters’, and called ‘Chuan-Xin-Lian (heart piercing lotus)’ in China, is a herbaceous plant in the family Acanthaceae.[9] It is not one of the original traditional Chinese Saracatinib ic50 herbs, since the record of its use in China can only be traced back to the 1950s.[10] However, it is believed to be able to clear away ‘heat’ and relieve ‘toxicity’, ‘cool the blood’ and ‘reduce swelling’, and is widely used for treating common cold, fever, sore throat, aphthous stomatitis, cough, diarrhoea, heat stranguria, skin sores and ulcers, venomous snake bite etc.[10] Andrographolide is a major bioactive chemical constituent of this plant, and exhibits

a broad range of biological activities, such as anti-inflammatory, antibacterial, antitumor, antidiabetic, antimalarial, and hepatoprotective.[9] Andrographolide and its derivatives have been used in China as oral, intro-muscular, and intravenous Dipeptidyl peptidase preparations since the 1970s, for treating common cold, pneumonia, bacillary dysentery, tonsillitis etc.[11] According to a statistical analysis in 2005, more than 3.7 million ampoules of andrographolide injections had been used in sampled hospitals of selected cities in China that year.[12] However, in April 2005, the Adverse Drug Reaction Monitoring Center of the China Food and Drug Administration (CFDA) published an Adverse Drug Reaction Notice that from January 1988 to March 2005, it received 17 cases of acute renal failure induced by andrographolide injections.

This constituted the VPC familiarization phase. Infants were then tested using the VPC at three delays: (1) immediately following familiarization (“Imm”), (2) two minutes following familiarization (“2 min”), and (3) 1 day after familiarization (“Day 2”). For each of these three VPC tests, infants were shown the familiar face next to a novel face for a total of 20 sec and the left or right position of the faces switched sides after 10 sec. At each VPC comparison

test, infants saw a unique face paired with the familiarization selleck kinase inhibitor face. The Day 2 visit began with the final portion of the eye-tracking experiment and concluded with the ERP paradigm. Infants were again calibrated to ensure successful gaze tracking with the Tobii monitor and then presented with the third and final VPC test comparison (Day 2). After the eye-tracking portion of the experiment, the ERP task began. Before fitting the child with the HCGSN, infants were familiarized to a new face. This face was presented 20 times for 500 ms in the center of the screen with a variable intertrial interval of no less than 1,500 ms.

EEG was then recorded as infants saw this newly familiarized face (“recent familiar”), the VPC familiarization face from Day 1 and Day 2 (“VPC”) and a third never-before-seen face (“novel”) presented in a semirandomized order such that for every three stimuli presented, these three faces each appeared once (so they were randomized within every set of three). This ensured GPCR Compound Library cell line an even number of presentations of each of the three stimuli. Stimuli were counterbalanced across participants, such that the “VPC” face for one set of infants would serve as the “recent familiar”

face for a second set of infants and the “novel” face for a third set of infants. From a separate room, an experimenter observed infant’s eye movements and attentiveness through a video camera mounted on top of the experimental monitor. Stimulus presentation was initiated only when the child was attending to the screen, and any trial where an infant’s attention shifted during image presentation was flagged and removed from later analysis. Images were presented until infants saw a maximum of 126 trials or until the infant became too fussy to continue. Nutlin-3 price Gaze data were collected at a sampling rate of 60 Hz throughout the testing session. Before the eye-tracking data were exported from the Tobii Studio program, areas of interest (AOIs) were drawn onto the stimuli, enabling the subsequent analysis of gaze data within these particular AOIs. A single AOI was created for each picture that encompassed the face and gray background and was labeled as familiar face or unfamiliar face. Each participant’s eye-tracking data were exported from Tobii Studio, with time samples identified in which gaze fell within one of the faces. These exported data files were run through a custom-made Python script (Python Programming Language; www.python.

Conclusion: In selected diabetic population, incidence of NDRD was 75% and all patients had type 2 DM. Wide spectrum of different categories of renal diseases in diabetics depend on usual prevalence of renal diseases in general population according to geographical and ethnic characterstics and underlying

diabetes mellitus has no bearing on development of specific type of NDRD. Patients with NDRD had shorter duration of diabetes and lesser prevalence of hypertension.None of the seven clinical and laboratory criteria including absence of diabetic retinopathy, considered buy INCB018424 atypical for a diabetic nephropathy patient, which led to suspicion of underlying NDRD, could strongly predict occurrence of the same. So renal biopsy is the only investigation presently available to make a definitive diagnosis of NDRD. GOPLANI KAMAL R1,2, KASWAN KAMAL K3, GERA DINESH N5, SHAH PANKAJ R5, VANIKAR ARUNA V6, PATEL HIMANSHU V4, GUMBER MANOJ R5, KUTE VIVEK B4, TRIVEDI HARGOVIND L7 1Shalby Hospitals, Ahmedabad; 2Hon.Associate Professor Civil Hospital Ahmedabad; 3Consultant Nephrologist, Narayan Hrudayala, Jaipur, India; 4Assistant Professor Nephrology, IKDRC-ITS,

Ahmedabad India; 5Professor, Dept. of Nephrology, IKDRC-ITS, Ahmedabad; 6Professor, Dept Of Pathology, IKDRC-ITS, Ahmedabad; 7Director, IKDRC-ITS, Ahmedabad Introduction: Rapidly progressive glomerulonephritis(RPGN) is one of the most calamitous conditions in the nephrology where patients can progress from normal renal function to end stage renal failure within weeks. Patients and renal survival is significantly dependent on early proper management. Recognition of proper etiology & extent of pathology Venetoclax in vitro by early renal biopsy is essential in advance to decide timely treatment of these patients for proper salvageability. Aim of the study: To study the epidemiology of RPGN

atour centre.To study the response of aggressive treatment modalities like cytotoxic drugs and plasmapharesis. Methods: This is a prospective study of profile of rapidly progressive glomerulonephritis. Cases admitted to our institute between Aug. 2008 to Dec. 2010 were included. Mean follow up duration was 209 +/-135 days.All patients were treated with Steroids+ Cyclophosphamide+/− selleck products plasmapharesis. Results: Of total 86 patients mean age 30.23 + 34.16 yrs. Male : Female ratio 1:1.Commonest presenting symptom was oligouria(76.92%) macroscopic hematuria in 86.54%, microscopic hematuria in 86.54%.Mean duration of illness before diagnosis was 21.19 + 35.8 days. Pauciimmune GN was the most common etiology with 24.41% followed by PIGN in 22.09%, Lupus in 17.44%, IgA in 15.11% and MPGN in 12.79%.ANCA negative pauciummune GN was equal in number to ANCA +ve GN. 75% required dialysis on presentation.Complete renal recovery was present in 41.86% while partial renal recovery was present in 30.23%, while 27.90% progressed to end stage renal disease. Plasma exchange was done in 22 patients out of which 12 had renal recovery.

Although there was no significant difference (r= 0.98) between cholesterol removal by resting and dead cells, most strains exhibited higher cholesterol removal when resting cells were suspended

in phosphate buffer (pH 6.8) compared to heat-killed cells (Fig. 1). Moreover, the amount of cholesterol removed by the cells during growth was significantly higher compared to the cholesterol removed by heat-killed and resting cells (P < 0.01). In this Selleck Crizotinib study, for all three cell types (growing, resting, and heat-killed cells), the highest cholesterol removal was by the B3 strain (23%, 14% and 10%, respectively). All of the strains produced more EPS in the presence of cholesterol than the strains grown without cholesterol during the 19-hr incubation period (Fig. 2). In other words, cholesterol significantly

stimulated the EPS production and the Pearson correlation coefficient was statistically significant (P < 0.01). It is remarkable that at the end of the 19- and 48-hr incubation periods, in the media containing 1 mg/ml oxgall, the B3 strain, which achieved maximum cholesterol removal to the values of 34% and 40%, respectively, had the highest EPS production (211 mg/l) capacity. Furthermore, the ATCC 11842 strain, which had the second highest EPS production capacity (200 mg/l), also had the second highest cholesterol removal rate after the B3 strain. For the immobilization study, among the five strains tested, the B3 strain, which had Pexidartinib cost the highest EPS production and cholesterol removal capacity, was selected. Observable differences were found in cholesterol removal by immobilized and free B3 cells (Table 3). For both of the incubation periods (19 hr and 48 hr), immobilized cultures exhibited higher cholesterol removal ability compared to the free

cells. The highest cholesterol removal (50%) was achieved by the immobilized B3 strain at the end of Tyrosine-protein kinase BLK the 48-hr incubation period. The viable cell counts in free and immobilized cultures at the end of the 19- and 48-hr incubation periods are shown in Table 4. After 19-hr incubation, in the PBS buffer solution containing 100 μg/ml cholesterol plus 3 mg/ml oxgall, the immobilized B3 culture contained 6.5 ± 0.2 × 103 cfu/ml, which represented 72% of surviving bacteria. In contrast, after 48-hr incubation, it contained 1.8 ± 0.2 × 102 cfu/ml, which represented a 51% survival rate. These results are higher than those observed with free cells. Coronary heart disease is one of the major causes of death and disability in many countries (21). Elevated levels of serum cholesterol is also a risk factor for the development of atherosclerotic vascular disease (22). Drug therapy for hypercholesterolemia includes fibrates, statins and bile acid sequestrants; however the undesirable side-effects of these compounds have caused concerns about their therapeutic use.

tb both induced T cells specific for the known epitope residing in TB10.4-P8 27, whereas P3 and P7 were

the main epitopes recognized following TB10.4 vaccination, in agreement with an earlier study (Fig. 1 and 215). Interestingly, although TB10.4 as a subunit vaccine does not induce T cells specific for the major CD4 epitope induced by infection (P8), TB10.4 has been shown to protect CB6F1 mice against an infection with virulent M.tb. This indicates that an M.tb infection does lead to some intracellular processing and presentation of P3 and/or P7 despite the low numbers of infection-driven P3- and P7-specific T cells. It also indicates that vaccines may not have to induce responses against dominant infection-driven T-cell epitopes in order to be protective. This may be important for future vaccine design as discussed below in the concluding remarks of the Discussion this website section. It has been demonstrated that post-translational modifications and native folding of Ag can alter immunogenicity

of a protein and even mask or unmask certain epitopes selleck inhibitor in an Ag compared with the recombinant version of the same antigen 29, 30. However, we found that immunization with native TB10.4 did not alter the epitope pattern compared to immunization with recombinant TB10.4 produced in E. coli (Fig. 3). In addition, TB10.4 is believed to be co-transcribed and secreted from both BCG and M.tb in a complex with Rv0287 19, 20. Complex formation of the related Ag CFP10-ESAT-6 has been shown to alter the structure, stability and function of these Ag 31, and to reduce their immunogenicity 32, 33. However, we showed that immunizing

with the native complex TB10.4-Rv0287 induced recognition of the same epitopes recognized after immunization with monomer TB10.4 and induced a similar level of IFN-γ production (Fig. 4). Furthermore, it was shown that boosting BCG with TB10.4 led to recognition of the dominant epitopes induced by both BCG and TB10.4, suggesting Cediranib (AZD2171) that the different epitope patterns after TB10.4 and BCG immunization were not due to mutually exclusive dominance between epitopes. BCG and M.tb encode two TB10.4-homologues, TB10.3 and TB12.9 34. Possibly, BCG or M.tb could induce T cells specific for P8 in TB10.3/TB12.9, and not TB10.4. However, only TB10.4 was predicted by RANKPEP (http://bio.dfci.harvard.edu/RANKPEP) 35 to have an MHC-II (I-Ad)-restricted epitope within P8 for the b and d haplotype-restricted CB6F1 mice, suggesting that the P8-specific CD4+ T cells observed in our study recognized P8 from TB10.4. Both BCG and TB10.4/CAF01 vaccines were taken up by DC and macrophages, but TB10.4/CAF01 was targeted by DC to a higher degree than BCG in line with results from Korsholm et al. 7 (Fig. 4). On the other hand, BCG was taken up efficiently by granulocytic Ly6-G expressing neutrophils, in agreement with a recent study by Abadie et al. 5.

In one report, NKT cells inhibited the selleck screening library differentiation of diabetogenic T cells into Th1 cells through contact-dependent but IL-4-independent manner 32. The discrepancy between this report and ours may come from several factors. First, the mouse strains are different (NOD versus B6). Second, we used NKT cells from cytokine knockout mice which affect the cytokine

production from NKT cell but not from CD4+ Th. Finally, the ratio of cell numbers of NKT:CD4+ T cells in in vitro assay was somewhat different: 2:1 in this report and 1:4 in our experiments. Different ratios would clearly affect the outcome of NKT cell-mediated Th regulation. The important role of Th17 cells in autoimmune encephalitis and arthritis requires the detailed evaluation of the specific mechanism by which NKT cells regulate these Th17-mediated autoimmune diseases. IL-4, IL-10, and IFN-γ have been suggested to be important in inhibiting

click here Th17 differentiation in an autoimmune encephalitis model using 2D2 cell transfer 26, but in this study they used blocking antibodies to evaluate the role of cytokines. These antibodies, however, blocked all cytokine signaling, not just the cytokines secreted from activated NKT cells. In addition to this, blocking antibodies also affect Th differentiation by themselves, i.e. anti-IFN-γ antibody treatment stimulate Th2 differentiation and anti-IL-4 antibody treatment induced Th1 differentiation 2. The predominant role of a cytokine-independent mechanism has also been suggested in an autoimmune encephalitis model in NOD mice 27. Therefore, the identity of the NKT cell-derived factors that regulate Th17 differentiation remains an open question. In this study, we found that contact-dependent mechanisms were predominantly involved in suppressing Th17 differentiation. To address the effect of cytokines derived from NKT cells, we used NKT cells deficient in specific cytokines, particularly the Th1 (IFN-γ)- and Th2 (IL-4 and IL-10)-associated cytokines, because Th1 and Th2 cytokines are known

to inhibit Th17 differentiation 1–3. All of the examined cytokine-deficient NKT cells suppressed CD4+ T-cell differentiation into Th17 cells (Fig. 1). The observation that IFN-γ production from activated NKT cells was dramatically reduced in the presence of Th17-promoting Phosphoprotein phosphatase cytokines (Fig. 2) suggests that the well-known IFN-γ-mediated inhibition of Th17 differentiation 1–3, 33 may not be effective in these cytokine environments. Moreover, the effective suppression of Th17 differentiation by IFN-γ-deficient NKT cells in our study confirmed the minor effects of IFN-γ in the Th17-promoting environments. Results from experiments using a transwell system (Fig. 3A and B) and culture supernatants from purified NKT cells activated with α-GalCer (Fig. 3C) strongly supported the idea that the NKT cell-mediated suppression of Th17 differentiation was predominantly dependent on cell contact.