Measurements were carried out intra-operatively after clamping and declamping the perforator vessels. In the post-operative period measurements LDK378 were carried out every hour for the first 48 hours and from 3rd to 7th for every 2 hours. These dates were compared to findings of clinical assessment. Several intra-operative measurements, during the clamping and declamping the different perforator vessels, revealed a high correlation for all parameters: Flow (r = 0.89, P < 0. 05), Velo (r = 0.92, P < 0. 05), SO2 (r =0.84, P <0. 05), and rHB (r =0.83 P < 0.05). Vessel occlusion

was detected in five cases, of which three were due to arterial thrombosis and two further FK506 cases were due to venous occlusion. Of the five cases, one flap loss caused by venous occlusion was noted. The O2C-device seems to be a reliable, objective, and non-invasive device for the monitoring of free flaps. Thus, it may improve flap survival rates by detecting vascular compromise at an early stage. © 2013 Wiley Periodicals, Inc. Microsurgery 33:350–357, 2013. “
“In brachial

plexus injuries, though nerve transfers and root grafts have improved the results for shoulder and elbow reconstruction, wrist extension has received little attention. We operated on three young patients with C5–C8 root injuries of the left brachial plexus, each operated upon within 6 months of trauma. For wrist extension reconstruction, we transferred a proximal branch of the

to flexor digitorum superficialis to the motor branch of the extensor carpi radialis brevis. Twenty-four months after surgery, all patients recovered some degree of active wrist motion, from full flexion to near neutral. Independent control of finger flexion and wrist extension was not observed. In C5–C8 root injuries of the brachial plexus, transfer of a flexor digitorum superficialis motor branch to the extensor carpi radialis brevis produces limited recovery. © 2012 Wiley Periodicals, Inc. Microsurgery, 2013. “
“Composite defects of bone and soft tissues represent a reconstructive challenge. Several techniques have been described in the medical literature; however, extensive composite defects should be reconstructed with microvascular free tissue transfer. The purpose of this report is to present the use of a composite latissimus dorsi and serratus anterior and rib free flap (LD-SA/rib) as an alternative procedure in patients who cannot undergo more commonly used vascularized bone-containing free flap reconstruction. Since January 2009, 12 patients have undergone bone and soft tissues reconstruction with a composite LD-SA/rib flap. In this case series, indications for LD-SA/rib reconstruction were large mandibular defects after oral cancer ablation, scalp defects, and lower extremity defects. All flaps survived entirely.

Eravani and S. Alizadeh (Pasteur Institute of Iran). Special thanks to Dr Nariman Aghaei Bandbon Balenga (Medical University of Graz) for helpful

discussion on neutrophil isolation. Financial support was this website provided by Iran Ministry of Health and Pasteur Institute of Iran. “
“Recurrent miscarriage (RM) is the occurrence of three or more consecutive miscarriages before gestational week 20 and is a condition that affects 1–3% of women [1]. RM can be classified into two categories: primary RM (no prior live birth) or secondary RM (three or more consecutive miscarriages following a live birth). In addition to genetic and anatomical factors causing RM, many studies have suggested that signs of autoimmunity and dysregulation of natural killer (NK) cell immunity characterize women with RM. Approximately 25 years ago, the first pilot studies on the use of intravenous immunoglobulin (IVIg) for the treatment of RM were conducted and reported a live birth rate of 80–82% [2, 3], which provided support to warrant further investigation in placebo-controlled trials. In 2006, a Cochrane review Selleckchem Apoptosis Compound Library of IVIg treatment for RM in

eight placebo-controlled trials with 303 RM patients was conducted, concluding that IVIg did not increase live birth rates when compared to placebo [odds ratio (OR) = 0·98; 95% confidence interval (CI) = 0·61–1·58] [4]. However, this review did not differentiate between primary and secondary RM patients. Separate analysis of these two subsets of RM patients may be necessary, as several studies have observed that secondary RM is a condition dominated by immunological risk factors when compared to primary RM, suggesting large heterogeneity between these two subgroups. Tumour necrosis factor (TNF)-α is a cytokine involved in the immune system’s inflammatory response. Piosik et al. analysed peripheral blood samples of RM patients taken at gestational week 5, and found that TNF-α levels were increased significantly in secondary RM patients compared to primary RM patients (P = 0·042) [1]. This indicates that Obeticholic Acid chemical structure secondary RM is a condition with an increased proinflammatory

response in early pregnancy. More evidence of the role of immunological factors in secondary RM has been reported in studies that have shown associations between secondary RM patients with specific maternal human leucocyte antigen (HLA) polymorphisms. Kruse et al. found that there was a significantly higher prevalence of the HLA-DRB1*03 allele in secondary RM patients compared with controls (OR = 1·8; 95% CI = 1·3–2·5) [5], whereas the allele was not increased in patients with primary RM. A previous pregnancy with a boy can be a risk factor for secondary RM. In general, maternal immune recognition of male-specific minor histocompatibility (HY) antigens expressed in male fetal and trophoblast cells is well tolerated, resulting in a live birth. However, pregnancy with a boy may prime the mother’s HY immunity.

burgdorferi genospecies. Therefore, we performed an analysis of the total lipid extracts of a wide spectrum of genospecies of B. burgdorferi sensu lato using thin-layer chromatography as well as Western blot and dot-blot assays. We show that ACGal is present in substantial quantities in all B. burgdorferi genospecies tested. Therefore, this molecule might improve the serological

click here detection of rarely pathogenic genospecies, and may be used as a protective vaccine regardless of the prevailing genospecies. Lyme disease (LD) is a multisystemic, often chronic infectious disease prevalent in Europe, North America, and Asia. In endemic areas, LD reaches an incidence of up to 160 cases per 100 000 (Berglund et al., 1995; Strle, 1999). The clinical manifestations are divided into early and late manifestations: early localized Z-VAD-FMK concentration disease is characterized by erythema migrans. Disseminated early

disease primarily encompasses neuroborreliosis, lymphocytoma, or myocarditis. Late manifestations predominantly comprise Lyme arthritis, acrodermatitis chronica atrophicans, and rarely late neuroborreliosis (Huppertz et al., 1999). LD diagnosis is based on the clinical signs and serodiagnosis using ELISA and confirmative immunoblots (Wilske et al., 2007). A number of Borrelia burgdorferi sensu lato genospecies are etiologic agents of LD causing early localized as well as early and late stages of disseminated disease: B. burgdorferi sensu stricto,

Borrelia afzelii, and Borrelia garinii. Furthermore, the OspA serotype Nintedanib (BIBF 1120) 4 of B. garinii, which has been associated with LD affecting the skin and CNS (Wilske et al., 1993), was recently delineated as a novel genospecies, Borrelia bavariensis (Margos et al., 2009). To the contrary, Borrelia spielmanii causes the localized stage while disseminated disease caused by this agent has not been reported as yet (Fingerle et al., 2008). Three further genospecies are rarely found in skin biopsies and only in single cases in CSF or cardiac tissue. The pathogenic potential of these genospecies, namely Borrelia bissettii (Fingerle et al., 2008; Rudenko et al., 2008), Borrelia valaisiana (Diza et al., 2004), and Borrelia lusitaniae (Collares-Pereira et al., 2004), remains unclear. Furthermore, eight genospecies of the group have been found only in ticks or in animals, for example Borrelia japonica (Kawabata et al., 1993), and are considered nonpathogenic for humans. We and others have identified 6-O-acylated cholesteryl β-d-galactopyranosides (ACGal) as the major glycolipids in B. burgdorferi sensu stricto, B. afzelii, and B. garinii (Ben-Menachem et al., 2003; Schröder et al., 2003; Stübs et al., 2009). On the other hand, Borrelia hermsii – the causative agent of relapsing fever – contains 6-O-acylated cholesteryl β-d-glucopyranosides (ACGlc) (Stübs et al., 2009).

In their setting, the co-injection of

LPS did not boost Ab production and the fact that the humoral response had undergone isotype switching was taken as evidence of CD4+ T-cell priming, which was confirmed by using T-cell-deficient mice. When targeting small amounts of antigen to DNGR-1 in the absence of adjuvant, we are unable to induce immunity as assessed by antigen-specific Th1, Th2 or Th17 differentiation or an anti-rat IgG response. Instead, we found that antigen targeting to DNGR-1 in the steady state, if anything, leads to Foxp3+ T-cell differentiation. see more This observation is consistent with the fact that our anti-DNGR-1 antibodies, like those of Caminschi et al., are unable to trigger detectable phenotypic or functional maturation of CD8α+ DC, thought to be a prerequisite for immunity 4, 9, 17. With our reagents, AZD4547 inducing an anti-rat IgG response in the absence of adjuvant was only possible when high amounts of antigen were injected. But even when pushing the system in that manner,

the response remained 2–3 orders of magnitude lower than the one induced in the presence of poly I:C. These data suggest that antigen targeting to DNGR-1 in the absence of adjuvant might lead to Ab production in certain conditions but that the process is inefficient and that DC activation by a potent adjuvant remains important for triggering of a strong humoral response. Thus, our data largely agree with those of Caminschi et al. and any differences might be quantitative and reflect the use of distinct targeting antibodies, possibly bearing different affinities for DNGR-1. The major difference between the two studies is the fact that Caminschi et al. found that the inclusion of adjuvant did not substantially boost Ab titers, whereas in our case, we see a massive increase. This discrepancy might be explained by the fact that Caminschi et al. used PAK6 LPS, which is a poor adjuvant in

comparison with poly I:C for antigen targeting approaches in which CD8α+ DC are the dominant APC (data not shown and 23). It has recently been proposed that human blood lineage-negative HLA-DR+ BDCA-3+ cells may encompass functional equivalents of mouse CD8α+ DC in mice 19. A genome-wide analysis of the transcriptome of different populations of mouse and human leukocytes supports this contention 41. If BDCA-3+ DC prove to have similar properties to the mouse CD8α+ DC population, those cells could become attractive targets for immune manipulation. In mice, targeting to DEC205 has been considered as the “canonical” way to direct antigens to CD8α+ DC. However, there is no evidence that this lectin is expressed on BDCA-3+ DC and additionally human DEC205 has been detected on a large spectrum of hematopoietic cells 3.

The idea that Treg have the capacity to specifically suppress Th1, Th2, or Th17 responses has gained ground in the past year and fits

well with the conclusions of the article 18. Recently, elegant studies have demonstrated that Treg respond to cues from their cytokine environment and develop into highly specialized suppressors of Th1, Th2, or Th17 responses. These tailored suppressive functions are induced in Treg by “mirroring” expression of transcription factors specific for the target population. Thus, Rudensky and colleagues 19 showed that Treg expressing high levels of interferon MAPK Inhibitor Library nmr regulatory factor 4 (IRF4), an essential transcription factor for Th2 cells, selectively suppress Th2 responses. Specific ablation of IRF4 in Treg leads to uncontrolled Th2 responses

with increased numbers of IL-4- and IL-5-producing CD4+ T cells, increased serum IgG1 and IgE, tissue infiltration, and autoimmunity. In a second study 20, the same group showed a similar mechanism for the specific suppression of Th17 responses. It is suggested that IL-6 and TGF-β, cytokines that induce Th17 differentiation, activate STAT3 in Treg leading to the acquisition of a Th17-specific suppression program 20. Again, the same transcription Roxadustat cost factor, STAT3, is used by both Th17 cells and Treg to induce or inhibit the Th17 response respectively. Deleting STAT3 in Treg led to uncontrolled Th17 responses and fatal intestinal inflammation 20. Finally, and perhaps most relevant to the current study 18, such a linked transcriptional program was also identified for the suppression of Th1 responses 21. In this case, IFN-γ induces T-bet, an essential transcription factor for Th1 generation in Treg, which in turn enables Treg

to attenuate Th1 responses. In this issue, Liu et al.18 convincingly demonstrate diminished IFN-γ responses and increased levels of IL-4 in AChR-immunized Mirabegron mice treated with IL-2 complexes. This result suggests that IL-2 specifically promotes the Th1 suppression program in Treg during myasthenia gravis development. It would be of interest to ask whether Treg isolated from IL-2-treated mice express higher levels of T-bet. Alternatively, IL-2 may preferentially expand an already existing T-bet-expressing Treg population during the AChR autoimmune response. It should be noted that in disease models where skewing Th1 to Th2 responses is therapeutically beneficial, such as in the myasthenia gravis model described by Liu et al. 18, it cannot be excluded that IL-2 directly influences the Th1/Th2 balance. The role of IL-2 in Th1/Th2 differentiation is still not fully understood. Early reports suggested that IL-2 facilitated the development of Th1 and Th2 cells in vitro, perhaps by ensuring their survival during the differentiation process. Using IL-2−/− T cells, we showed that IL-4 and IFN-γ production is deficient after antigenic stimulation in vitro22.

Data are presented as mean ± STD of triplicate measurements. (B) The IL-2 secretion (taken from Fig. 1C) of TCR-transduced hybridoma cells does not correlate with TCR on-rate determined by SPR (see Materials

and methods) [1]. (C) gp209- 2M:HLA-A2 tetramer staining of hybridoma cells expressing gp209-specific TCRs without (top) or with (bottom) co-expression of CD8. (D, E) Tetramer decay rates were determined at 4°C by adding an anti-HLA-A2 blocking antibody to hybridoma cells expressing the indicated gp209-specific TCRs without (D) and with https://www.selleckchem.com/products/pf-562271.html (E) coexpression of CD8 that was previously stained with gp209–2M:HLA-A2 tetramer. (F) IL-2 secretion (taken from Fig. 1C) was plotted vs. the gp209–2M:HLA-A2 tetramer decay rate of hybridoma cells co-expressing gp209-specific TCR and CD8. The low R2 value and large p value indicates the lack of correlation between the two

variables. In panels B and F, only IL-2 secretion at a representative peptide concentration (8.0 μM) is shown; using other peptide concentrations yielded similar results (see Materials and methods and Supporting Information Table 1). Figure S2. Determination of 2D kinetic parameters. (A-E) A broad range of 2D effective affinities of TCR–pMHC interactions measured by micropipette adhesion frequency assay. Data shown in this figure are complementary to those shown in Fig. 3A; FG-4592 research buy combined, they constitute the 2D affinity measurements of the entire panel of TCRs expressed on CD8- hybridoma cells when interacting with gp209- 2M:HLA-A2 complexes. Forskolin in vitro Experiments were conducted as described in Fig. 3A except that different TCR-expressing cell lines were used. The data shown (including adhesion frequencies and surface densities of TCR and pMHC) are for (A) 16LD6, (B) K4H5, (C) 5CE2, (D) L2G2, and (E) W2C8 hybridomas. Each point represents mean ± SEM of Pa measured from 2–6 pairs of hybridomas cells and gp209–2M:HLA-A2 coupled RBCs. (FJ) Rapid dissociation of 2D TCR–pMHC bonds as measured by thermal fluctuation assay. Data in this figure are complementary to those shown in Fig. 4A; combined, they constitute the 2D off-rate

measurements of the entire panel of TCRs expressed on CD8- hybridoma cells when interacting with gp209–2M:HLA-A2 complexes. Experiments were conducted the same way as in Fig. 4A except that different TCR-expressing cell lines were used. Data shown are for (F) 16LD6, (G) K4H5, (H) 5CE2, (I) L2G2, and (J) W2C8 hybridomas. Triangle symbols represent outliers that were not included in linear regression analysis. (K) The 2D effective on-rates show a broad dynamic range. 2D onrates of TCR–gp209–2M:HLA-A2 association (open bars) were calculated based on 2D affinities and off-rates. The on-rates span a 5-log range across the six TCRs with a descending potency to respond to gp209–2M. The on-rate of the gp209–2M:HLA-A2– CD8 association (closed bar) was calculated similarly as that of the TCR-gp209- 2M:HLA-A2 association.

The dramatic increase in CD163 expression in HEK293 CD163-transfected cells in contrast to the untransfected cells (Fig. 5E) was reflected in a significantly higher ML uptake/internalization increase (Fig. 5F). No major difference in the percentage of infected cells was found in comparison with the transfected and untransfected HEK293 cells either 2 or 16 h postinfection. However, ML association (not shown) and uptake (Fig. 5F) were more

efficient in CD163-transfected cells than untransfected cells after 16 h of culture (9807 ± 235 ML MIF in untransfected cells versus 22811 ± 1724, p < 0.001). As a whole, these data strongly suggest that CD163 functions as an alternative Protein Tyrosine Kinase inhibitor receptor for ML entry into host cells. To verify selleck chemicals llc if CD163 is involved in iron uptake by LL cells, AFB-negative BT skin lesions (n = 6) and LL skin samples (n = 9) showing bacteriological index > 5 (Wade staining, Fig. 6A) were submitted to Perls’ Prussian blue reaction. Positive iron deposits were detected intracellularly in foamy, bacilli-loaded macrophages (Fig. 6B). In BT samples, epithelioid macrophages occupying the core of the typical tuberculoid granuloma stained completely negative (Fig. 6C). Small foci of iron deposits in vaguely differentiated macrophages were seen in BT lesions. In this study, past descriptions that foamy macrophages predominate

in LL lesions among a plethora of other macrophages were all but confirmed. Immunohistochemical analysis of polar LL lesions demonstrated that the majority of these cells were positive for CD68, CD163, and IDO. Interestingly, after 6 days of culture, CD68+CD163+IDO+ markers were identified Fossariinae in cells isolated from LL lesions, suggesting that a part of these cell populations maintains the same phenotype while simultaneously discarding their intracellular bacilli and foamy appearance. In vitro studies have demonstrated that ML provides both positive and negative regulatory signals even

when TCRs are the trigger stimuli [22]. Although live ML seems to be more efficient at inducing ML phagocytosis, heat-killed ML is more effective at inducing T-cell activation [23]. Moreover, we herein describe that CD163 scavenger receptor type 2 is induced by both live and dead ML. The increased CD163 expression triggered by ML positively correlated with IDO and CD209 expression. The role of CD163 as a bacterial receptor was first described by Fabriek et al. [16], who considered that bacterial and cellular recognition constitutes unifying and perhaps even primordial functions of the scavenger domain as well. Both the CD163 blockade and the cythocalasin B treatment were found to inhibit ML uptake by human monocytes, leading to the conjecture that CD163 contributes to ML entry into host cells and that CD163 activity is regulated by the phagocytic machinery.

Theoretically, glycosuria is more frequent in chronic kidney disease (CKD). However, the consequence of glycosuria is little known. In contrast, impaired renal tubular reabsorption could prevent renal tubules from the protein injury of glomerular filtrates. We would thus click here study glycosuria and its association with renal outcome in non-diabetic

CKD patients with proteinuria. Methods: We recruited 988 non-diabetic CKD stage 3 to 5 patients with proteinuria between 2002 and 2009. Glycosuria was defined as more than one measurements of urine glucose +∼++++ by dipstick during the follow-up period and at least once in the first three tests. Results: The mean age was 60.9 years, estimated glomerular filtration rate (eGFR) was 19.1 mL/min per 1.73 m2 and urine protein-to-creatinine ratio was 1962 mg/g. Percentage

of glycosuria was 2.4%, 12.8% and 46.9% in non-diabetic CKD stage 3, 4 and 5, respectively. It was also higher in those Navitoclax datasheet with heavy proteinuria. In multivariate logistic regression, glycosuria was associated with eGFR, proteinuria, hemoglobin, albumin, and phosphorus. In survival analysis, glycosuria was associated with a decreased risk for end-stage renal disease (ESRD) (hazard ratio = 0.79; CI = 0.63–0.98; p = 0.034) and selleck chemicals llc for rapid renal function progression (odds ratio = 0.64; CI = 0.43–0.95; p = 0.027); but glycosuria was not associated mortality or cardiovascular event. Conclusion: Glycosuria was associated better renal outcome in non-diabetic CKD stage 3–5 patients with proteinuria. This may indicate that impaired renal tubular reabsorption of filtered protein is associated with less renal function progression. IIMORI SOICHIRO, NISHIDA HIDENORI, OKADO TOMOKAZU, RAI TATEMITSU, UCHIDA SHINICHI, SASAKI SEI Department

of Nephrology, Tokyo Medical and Dental University Introduction: Treatment with erythropoietin stimulating agents (ESA) is an effective but costly therapy for CKD patients with renal anemia. On the other hand, correction of iron deficiency (ID) with iron supplementation can reduce the severity of renal anemia efficiently and inexpensively. We investigated the changes in anemia and iron status, management measures for renal anemia, and their association with cardiovascular (CV) risk in newly visited CKD patients for a one year follow-up period. Methods: We prospectively evaluated the risk of CV events in 951 newly non-dialysis CKD G2-G5 patients followed in 16 nephrology centers.

[37] Collectively, these studies demonstrate that iron uptake from ferrioxamine is mediated through the reductase/permease system.[37, 38] More recently, we were

able to identify the FOB1 and FOB2 as two closely related genes that encode cell surface proteins involved in binding ferrioxamine to R. oryzae cell surface.[39] Attenuation of expression of these two genes results in compromising the ability of R. oryzae to take up iron from ferrioxamine in vitro and reduces virulence in a deferoxamine-treated mouse model of mucormycosis.[40] A hallmark of mucormycosis is the universal propensity of the infection to invade blood vessels.[1] The Mucorales angioinvasion capabilities likely contribute to the capacity of the organisms to haematogenously disseminate to learn more other target organs. Therefore, interactions of invading organisms with endothelial cells and extracellular matrix proteins lining blood vessels represent a critical step in the progression of the disease. Earlier studies demonstrated the ability of Mucorales to bind Selumetinib cell line to extracellular

laminin and type IV collagen[41] as well as human umbilical vein endothelial cells.[42] Moreover, Mucorales appear to damage endothelial cells in vitro via a mechanism that involves the induction of their own endocytosis by the mammalian cells.[42] This endocytosis process is mediated by the binding of Mucorales to a mammalian Glucose Regulated Protein with the molecular weight of 78 kDa (GRP78).[43] Interestingly, only germlings of R. oryzae

bind to GRP78 and not spores, thereby fitting the notion that germlings are likely responsible for the haematogenous dissemination Amisulpride during mucormycosis. Thus far in fungal infection, GRP78 appears to be a unique host cell receptor since neither Candida nor Aspergillus bind to this protein during invasion of host tissues.[43] GRP78 is a heat shock protein that is mainly found in the endoplasmic reticulum acting as a chaperon for facilitating proper protein folding and targeting misfolded proteins for proteosome degradation.[44] It also plays an important role in endoplasmic reticulum Ca2+ homeostasis and in serving as a sensor for stress.[45] Finally, GRP78 was reported to be antiapoptotic and plays critical cytoprotective roles in early embryogenesis, oncogenesis, neurodegenerative diseases and atherosclerosis.[46] Fitting with the concept of GRP78 being a stress-related protein is the finding that GRP78 is overexpressed on the host cell surface when endothelial cells exposed to elevated concentrations of glucose and iron consistent with those seen during hyperglycaemia and DKA. This elevated GRP78 expression results in increased ability of R. oryzae to invade and damage endothelial cells in a receptor-dependent manner.[43] More recently, the Mucorales ligand that binds to GRP78 was identified as the spore coat protein homologs (CotH).

The present data clearly demonstrate that lactobacilli can modulate the cytokine induction profiles in hPBMC of allergic subjects in vitro. This modulation was most obvious in an increase in innate cytokine induction and a decreased synthesis of the Th2 cytokine IL-13 observed for all tested strains. Based on the present study, strains B1836, B2261,

the mixture of B2261 and B633, and B633 alone could be chosen as most promising probiotic strains because of their stronger inhibition potential of IL-13 induction and higher induction of IFN-γ and IL-12 compared with the other tested strains. Furthermore, the analysis presented here provides a suitable model to compare candidate probiotic strains www.selleckchem.com/products/gsk2126458.html find more for their

immunomodulating properties in vitro in a Th2-skewed population and can even be used outside the pollen season, which makes this methodology a useful screening model. We thank Sovianne ter Borg for technical assistance, ZGV (Gelderse Valley Hospital; Ede, the Netherlands) for providing patient-related data, Dr H. Verhoef and J. Veenemans for their expert statistical advice and Dr H. Yssel is kindly thanked for supplying the Yssel supplement. “
“Chronic inflammatory T-cell-mediated diseases such as inflammatory bowel disease (IBD) are often treated with immunosuppressants including corticosteroids. In addition to the intended T-cell suppression, these farmacons give rise to many side effects. Recently, immunosuppressive phospholipids have been proposed as less-toxic alternatives. We aimed to investigate the immunoregulatory capacities of the naturally occurring phospholipid phosphatidylinositol (PI). Systemic PI treatment dramatically reduced disease severity and intestinal inflammation in murine 2,4,6-trinitrobenzene sulfonic acid (TNBS) colitis. Moreover, PI Loperamide treatment inhibited the inflammatory T-cell response in these mice, as

T cells derived from colon-draining LN of PI-treated mice secreted less IL-17 and IFN-γ upon polyclonal restimulation when compared to those of saline-treated mice. Further characterization of the suppressive capacity of PI revealed that the phospholipid suppressed Th cell differentiation in vitro irrespective of their cytokine profile by inhibiting proliferation and IL-2 release. In particular, PI diminished IL-2 mRNA expression and inhibited ERK1-, ERK-2-, p38- and JNK-phosphorylation. Crucially, PI did not ablate Treg differentiation or the antigen-presenting capacity of DCs in vitro. These data validate PI as a pluripotent inhibitor that can be applied mucosally as well as systemically. Its compelling functions render PI a promising novel physiological immune suppressant.