We evaluated the clinicopathological
factors between the progression and the non-progression groups. Systolic, diastolic, and mean blood pressures were significantly higher in the progression group. Degree of hematuria was not associated with CKD progression. Segmental glomerulosclerosis and tubular atrophy/interstitial fibrosis characterized advanced risk for CKD progression. CKD selleck products stage did not progress in cases of mild pathological activity without ACEI/ARB. The baseline renal function, proteinuria, hypertension, the degree of mesangial and endocapillary hypercellularity, and values of IgA at biopsy were not associated with CKD progression during the three year follow-up. Proteinuria and hematuria decreased, and serum albumin increased significantly due to treatment regardless of CKD progression. Conclusion: We can protect renal function by adequate treatment at least for a three year follow-up period after
biopsy, despite high disease activity of IgAN indicated by proteinuria, hematuria, decrease of estimated GFR, and active pathological findings. Further follow-up must be needed to detect predictors associated with long-term renal prognosis. Suzuki Keisuke, Miura Naoto, Imai Hirokazu Aichi Medical University School of Medicine Background: This retrospective study was designed to estimate the clinical remission (CR) rate of tonsillectomy plus steroid pulse (TSP) therapy in patients with IgA nephropathy. Methods: Based on 292 of 302 patients with IgA nephropathy treated at 11 Japanese hospitals, we constructed AZD1208 mouse heat maps of the CR rate at 1 year after TSP with the estimated glomerular filtration rate (eGFR), grade of hematuria, pathological grade, number ID-8 of years from diagnosis until TSP, and age at diagnosis on the vertical axis and the daily amount of urinary protein on the horizontal axis. Results: The first heat map of eGFR and urinary protein showed that the CR rate was 71 % in patients with eGFR greater than 30 ml/min/1.73 m2 and 0.3–1.09 g/day of urinary protein. However, the CR rate in patients with more than 1.50 g/day of urinary protein was approximately 30 %. The
second heat map of grade of hematuria and urinary protein revealed that the CR rate is 72 % in patients with more than 1? hematuria and 0.3–1.09 g/day of urinary protein; however, it was 28.6 % in patients with no hematuria. The third heat map of pathological grade and urinary protein demonstrated that the highest CR rate was 83 % in patients with pathological grade I or II disease and less than 1.09 g/day of urinary protein, as opposed to 22 % in patients with pathological grade III or IV disease and more than 2.0 g/day of urinary protein. The fourth heat map of the number of years from diagnosis until TSP and urinary protein revealed that the former did not influence the CR rate in patients with less than 1.09 g/day of urinary protein. However, in patients with more than 1.
82 We then demonstrated that RTP4 was also expressed in the uterine endometrium, which was surprising because expression of this gene was initially thought to be confined to olfactory neurons. Furthermore, in vitro treatment with IFN-τ increased RTP4 expression by a cell line derived from the uterine glandular
epithelium.82 It is not difficult to imagine potential roles for a chemosensory receptor transporting protein in the uterus during early pregnancy because chemokines are proposed to aid in trophoblast attachment and invasion.36 The chemokine CXCL10 was upregulated in the endometrium of pregnant ewes, Selleckchem KU-60019 and the receptor (CXCR3) was localized to the trophectoderm.83 Moreover, chemotaxis assays demonstrated that CXCL10 regulates migration and/or distribution of PBMC in the uterus during early pregnancy. Perhaps RTP4 affects chemokine receptors during early pregnancy to recruit immune cells to the pregnant endometrium.84 Further studies are needed to determine the role(s) of RTP4 in the endometrium during early pregnancy. What this experiment did reveal, however, was that gene expression in PBL during early pregnancy provided a novel and non-invasive mechanism to
identify new genes regulated in the uterus during early pregnancy. We hypothesize that by profiling gene expression patterns in PBL, we may be able to identify expression patterns associated with successful and unsuccessfully pregnancy outcome. By virtue of Oxymatrine the differences in placental structure 5-Fluoracil cost and hormonal signaling from the conceptus, it is likely that early pregnancy in cattle and humans present some very unique challenges for the maternal immune system. However, examination of immune responses to early pregnancy in these species does suggest there are some similarities. This is especially the case during the very early stages of embryo development in the uterus prior to the formation of a functioning hemochorial placenta. During this stage of pregnancy, blastocysts of both species are dependent upon uterine secretions for nutrition, they both
must attach to the endometrial epithelium, and they first encounter the endometrial mucosal immune system. The idea that early pregnancy in humans and ruminants may share more similarities than later pregnancy is supported by the elegant work of Knox and Baker18 showing that genes involved in early placental development are evolutionarily ancient compared to those involved in mature placental function. Figure 1 illustrates that early conceptus-immune interactions occur on a background of a progesterone-primed endometrium that exhibits selective immunosuppression. Conceptuses of both species secrete factors that extend the lifespan of the CL, and these factors affect immune cell function in the endometrium and in the peripheral blood.
The cumulative MIC percentage curves of the six antifungal agents for dermatophytes are shown in Figure 1. For two major causes of dermatomycoses, T. rubrum and T. mentagrophytes, MIC ranges of non-azole agents were narrower than those of azole agents. The MICs of total dermatophytes showed the same tendency (solid line). Unexpectedly, there were marked differences between T. rubrum and T. mentagrophytes in the MIC ranges of ketoconazole
and bifonazole. Table 4 presents a summary of the FIC indexes of 27 clinical dermatophyte isolates. Synergistic interactions were observed in 7 of 27 strains with FIC indexes of ≤0.5, additive interactions in 16 isolates with FIC indexes >0.5 ≤ 1 and four isolates had FIC indexes of GS-1101 research buy 2 (no interaction). In total, the combination of amorolfine and itraconazole had synergistic or additive effects in 23 clinical isolates (85%), and no antagonistic effects were detected. In the present study, we observed differences between T. rubrum and T. mentagrophytes in the MIC ranges of azole agents (ketoconazole and bifonazole),
T. rubrum being more sensitive than T. mentagrophytes to these azoles (Fig. 1). Previously, Barros et al. reported that there were no significant differences between T. rubrum and T. mentagrophytes in the efficacies of any of the drugs they tested (fluconazole, itraconazole, griseofulvin and terbinafine) . Santos et al. also reported no significant differences between MIC values of various antifungals
(fluconazole, itraconazole, griseofulvin, terbinafine, ketoconazole and cyclopiroxamine) in T. rubrum and T. mentagrophytes .That our results click here do not match those previously reported indicates that antifungal susceptibility may differ among populations; further studies of MIC values are therefore required even in these major dermatophytes. The MIC ranges of the non-azole agents amorolfine, terbinafine and butenafine against Trichophyton PD184352 (CI-1040) spp. were relatively narrow compared to those of azole agents (Fig. 1; Table 2). One possible explanation for this finding concerns the mechanisms of these drugs. Each azole inhibits one pathway of the ergosterol constructional system, whereas the morpholine agents act on two enzymes involved in ergosterol construction . Because the probability that variations in two enzymes will occur simultaneously is low, different positions of action may result in non-azoles such as amorolfine having more stable antifungal effects than azoles. Minimum inhibitory concentrations varied widely among non-dermatophyte strains (Table 3). In particular, all antifungal agents showed high MICs in Fusarium spp. The variation of susceptibility seen in dermatophytic and non-dermatophytic fungi indicates the necessity to identify the causative fungi to enable appropriate selection of effective antifungal drugs in each case and to avoid development of resistance [31-33].
We previously demonstrated that IC negatively regulates TLR4-triggered inflammatory
response in macrophages through FcγRIIb 27. We here demonstrate that in the presence of IC, FcγRIIb overexpression promotes resistance of immature DCs to TLR-triggered maturation induction and also increases DC tolerogenecity. Accordingly, IC-stimulated, FcγRIIb-overexpressing DCs (DC-FcγRIIb) can downregulate immune response more significantly both in vitro and in vivo, thus attenuating the progression of disease in lupus-prone mice. To investigate whether IC/Ig could inhibit TLR-induced maturation of DCs via FcγRIIb, Tamoxifen immature DCs derived from WT or FcγRIIb−/− mice were incubated with IC (OVA plus anti-OVA)/Ig (anti-OVA) for 24 h before these DCs were stimulated with LPS or CpG ODN for another 24 h. As for WT DCs, IC alone (whereas not Ig) slightly upregulated the expression of I-Ab, CD40, CD80
and CD86. Interestingly, IC pretreatment significantly inhibited the LPS or CpG ODN-induced upregulation HDAC inhibitor drugs of I-Ab, CD40, CD80 and CD86 expression, and Ig pretreatment significantly inhibited the LPS-induced upregulation of the four molecules and the CpG ODN-induced upregulation of CD80 and CD86 expressions (Fig. 1A). In contrast, neither IC nor Ig pretreatment had significantly inhibitory effect on the LPS or CpG ODN-induced upregulation of I-Ab, CD40, CD80 and CD86 expression on FcγRIIb−/− DCs (Fig. 1A). These data indicate that FcγRIIb mediates the inhibitory effect of IC/Ig above. IC alone could stimulate WT DCs as well as FcγRIIb−/− DCs to secrete TNF-α and IL-1β to some degree; however, IC pretreatment obviously suppressed LPS or CpG ODN-induced TNF-α and IL-1β secretion from WT DCs (Fig. 1B). In contrast, IC pretreatment could not suppress TNF-α and IL-1β secretion by LPS-stimulated FcγRIIb−/− DCs, and even promoted TNF-α and IL-1β secretion by CpG ODN-stimulated
FcγRIIb−/− DCs (Fig. 1B). OVA alone had no effect on the phenotype and cytokine ADP ribosylation factor secretion of WT DCs and FcγRIIb−/− DCs with or without stimulation with LPS, CpG ODN (data not shown). Considering that the Ig (anti-OVA mAb) we used, also exhibited inhibitory effect on LPS-induced DC maturation (in a similar manner to IC), we speculated that anti-OVA mAb might have some aggregated Ig, because aggregated Ig has a higher binding affinity to FcγRIIb than monomeric Ig. Therefore, we compared the differences between monomeric and aggregated Ig. As expected, the aggregated Ig significantly inhibited WT DCs to express I-Ab and CD40 and to secrete TNF-α in response to LPS stimulation, whereas monomeric Ig did not. However, neither aggregated Ig nor monomeric Ig had such inhibitory effect on LPS-induced FcγRIIb−/− DC maturation (Supporting Information Fig.
Human peripheral blood CD4+ T cells were stimulated with anti-CD3, IL-2, and IL-4 under conditions previously determined to optimally induce IL-10-Treg cells . The expression of Foxp3 and IL-10 in the presence or absence of 1α25VitD3 was determined by flow cytometry. 1α25VitD3 at 10−6 M led to an increase in Foxp3 expression as compared with control cultures (No VitD3), whereas lower doses of 1α25VitD3 minimally affected Foxp3 expression. In contrast, Selleckchem Seliciclib maximal IL-10 induction was observed, as expected, at 10−7 M and 10−8 M 1α25VitD3 . This response was confirmed
using a panel of donors. A statistically significant increase in the frequency of Foxp3+ T cells was observed at 10−6 M, but not at 10−7 M 1α25VitD3, while significant induction of IL-10+ T cells was seen at 10−7 M, but not at 10−6 M (Fig. 1A). In summary, 1α25VitD3 enhances both the percentage of Foxp3+ cells and the expression of Foxp3 transcripts (data not shown), but at a distinct concentration of 1α25VitD3 than required for optimal IL-10 induction.
In our early studies, cells were analyzed for expression of Foxp3 and IL-10 independently by flow cytometry. To confirm and extend the finding of differential effects of 1α25VitD3 on these molecules, a protocol for costaining was developed. CD4+ T cells were cultured with 10−6 M or 10−7 M 1α25VitD3 and then restimulated with anti-CD3 and IL-2 for 16 h and analyzed for expression of IL-10 and Foxp3 by secretion assay and then intranuclear staining. In two representative see more donors, shown in Figure 1B, virtually no (≤0.2%) cells stained positive for both Foxp3 and IL-10 in the presence of 10−7 M 1α25VitD3. When cells from a panel of healthy donors were screened, we observed that cell cultures preferentially expressed a high frequency of Foxp3+ cells and low levels of IL-10, or conversely Mephenoxalone low Foxp3 and a high frequency of IL-10+ cells in response to culture with 1α25VitD3 (Fig. 1B and C). Since Foxp3 expression may not always reflect inhibitory function, the functional consequences of 1α25VitD3 modulation of
Foxp3 versus IL-10 expression by human CD4+ T cells was next investigated. CD4+ T-cell lines generated from the same donor in the presence of either high (10−6 M; Foxp3-promoting Treg conditions) or lower (10−7 M; IL-10-Treg favoring conditions) concentrations of 1α25VitD3 were tested for their capacity to inhibit the proliferation of autologous, naïve CFSE-labeled responder T cells. Both populations showed comparable inhibitory activity (Fig. 2A). The suppression by cells generated with 10−7 M 1α25VitD3 could be diminished by the addition of anti-IL-10 receptor antibody to the co-culture, while in T-cell cultures generated with 10−6 M 1α25VitD3, the antibody had little effect (Fig. 2B), suggesting both IL-10-dependent and IL-10-independent mechanisms of suppression existed in the two different populations.
Several trials have clearly shown that intensive treatment of elevated BP lowers the risk of microvascular disease, CVD and mortality in type 2 diabetes (refer to systematic reviews of.4,16,17,64 The UKPDS has been the largest long-term study to compare the effects of intensive versus less intensive BP control in hypertensive people with type 2 diabetes. In this 9-year study of 1148 people, allocated to tight BP control (n = 758) or less tight control (n = 390), mean BP was significantly reduced in the tight control group (144/82 mm Hg), compared with the group assigned to less tight control https://www.selleckchem.com/products/ABT-263.html (154/87 mm Hg) (P < 0.0001). The study showed that microvascular endpoints, including the development BMN 673 of
microalbuminuria or overt diabetic kidney disease, were reduced by 37% in the intensive control group (P < 0.01).8 In this study, captopril and atenolol were used in equihypotensive doses and each drug attenuated the development of microvascular complications to a similar degree over 10 years.65 Elevated BP was identified as one of the major risk factors associated with a decline in kidney function and increase in albuminuria in a long-term non-interventional prospective study of 574 people with type 2 diabetes who were normotensive and normoalbuminuric (based on dipstick) at the start of the study.66 Those with
elevated BP (>95 mm Hg) had an almost 10 fold increased risk of developing microalbuminuria compared with those with lower BP over the average 8 year follow-up period. Recent analysis of the BP arm data of the ADVANCE Trial67 by Galan et al.68 has indicated that lower achieved follow-up (median 4.3 years) systolic blood pressure levels were associated with progressively lower renal event rates to below this website 110 mm Hg. These studies support the concept that arterial hypertension plays a pivotal role in contributing to kidney damage in type 2 diabetes, across the range of albumin excretion from
normal to micro- to macroalbuminuria. The studies also show that the rate of GFR decline can be successfully lowered in people with type 2 diabetes by effective antihypertensive therapy, however, the systematic review by4 considered that a 72% drop in clinical proteinuria noted in relevant trials was unlikely to be caused by the small difference in the BP between treatment groups and is consistent with renoprotective effects of ACEi. In people with type 2 diabetes antihypertensive therapy with ARB or ACEi decreases the rate of progression of albuminuria, promotes regression to normoalbuminuria, and may reduce the risk of decline in renal function (Evidence Level I – Intervention). A large number of systematic reviews and trials have examined antihypertensive therapy using ACEi and ARBs in people with type 2 diabetes. A summary of relevant studies is shown in Table A3 with findings of key studies described in the text below.
On average, 25% of macrophage-associated conidia are phagocytosed after 1 h, 16% of these cell-associated conidia are killed after
4 h and conidial germination was inhibited in more than 95% of the conidia of A. fumigatus. Comparable studies on zygomycetes would gain insights into the clearance of the fungal burden and forecast the potential of zygomycetes as causative agents of emerging fungal diseases. Moreover, transcriptomic analysis will help to understand the virulence and survival mechanism of the fungi when it confronts macrophages, e.g. the role of chromatin buy Sirolimus remodelling as a central regulator of survival strategies which facilitates a reprogramming of cellular energy metabolism in macrophage-internalised fungal cells and provide protection against DNA damage as shown for Candida glabrata. Many studies have established that virulence factors can be differentially expressed as a function of experimental conditions,
but clinical isolates of Cryptococcus neoformans behave differently under the same experimental conditions, a diversity that could participate in the variable outcome of infection in humans. It has been hypothesised that the survival strategies for soil-borne, potentially human pathogenic fungi (e.g. C. neoformans) after ingestion by macrophages and amoebae were similar. Consequently, selleckchem it will be worthwhile to compare the mechanisms of phagocytosis with amoebae which served as interacting partners in the environment resulting in a training of the fungal pathogen to successfully cope with the amoeboid immune cells of the human immune system towards adaption to the human host during evolution. Just recently, the whole genome of Acanthamoeba castellanii (Ac) was determined, the first representative from a solitary free-living amoebozoan. Ac utilises a diverse repertoire of predicted
pattern recognition receptors, many with predicted orthologous functions in the innate immune systems of higher organisms. The exploration of the fantofarone connection between both, receptors of amoebae and immune cells will shed light into the evolutionary origin of the interplay between fungal pathogen and innate immune cells. This work was financially supported by the Deutsche Forschungsgemeinschaft (DFG) Jena School for Microbial Communication (JMRC project #66) and within CRC/TR 124 FungiNet: project Z1 to KV. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. We express our gratitude to Paul M. Kirk (Royal Botanic Gardens Kew, UK) for providing the numbers of species for the subphyla and orders of the zygomycetes. The authors declare that no conflict of interest exists. “
“This multicentre observational study evaluated the feasibility, efficacy and toxicity of antifungal combination therapy (combo) as treatment of proven or probable invasive fungal diseases (IFDs) in patients with haematological malignancies.
The units identified by the Relational Coding Scheme represent different patterns of mutual adjustment
between partners and therefore the interaction corresponds to a sequence of episodes defined by an action of a partner followed by an selleck compound opportunity to act for the other. To take an oral conversation as an example, one partner talks and at the same time provides the other with a variety of opportunities to reply. The partner can reply in a way that follows on from the other’s content, at the same time bringing into the conversation something new; so, their communicative episode can be considered to be coregulated in a reciprocal manner. According to the coding system, the coregulation forms we observe in a communicative process vary from unengaged to unilateral to asymmetrical to symmetrical coregulation, and breakdowns in communication can also occur (see Table 1 for the operational definitions). For the purpose of the
present study, the symmetrical code was divided into three subcodes—affect, Selleck NVP-LDE225 action, and language, respectively—so, the original scheme has been partly modified (see Table 1). Coding was done continuously from the video by two independent coders and the coregulation states were identified by segmenting joint activity into units, lasting at least 3 sec, corresponding to the above categories. The onset time of each code was also recorded. From the coding records, durations of each category were computed and used as measures for the analysis. Because of slight variations in the session length, the raw durations in each session were transformed into proportions according to the duration of that session (proportional durations). Proportions of categories of less than .5% were excluded from the data analysis. Interobserver reliability was calculated on 30% of the entire data set. To be specific, 30% of sessions were randomly sampled for each dyad from each of the following
three age periods: 44–64, 65–88, and 85–104 weeks (Bakeman & Gottman, 1986, p. 77). Kappa assessments were based on whether two independent Astemizole coders agreed about the category coded in each second. Across all categories, the average kappa was not less than 80% in each of the three periods. Hierarchical random effects modeling (Goldstein, 1995, 2003; Snijders & Bosker, 1999) was used to test the advanced hypotheses. MLwiN statistical software was used to implement all the models (Goldstein et al., 1998). In the present study, data were collected on a two-level hierarchy (Rasbash, Steele, Browne, & Prosser, 2005), with the dyads at the higher level (level 2) and the set of measurement occasions (i.e., the infant’s age in weeks) for each dyad at the lower level (level 1).
brasiliensis model. The CCR3 receptor would be a logical target for blockade or deletion, because this is the only known receptor for the murine eotaxins. This might be performed in conjunction with inhibition of the C5a receptor, and as previously (75,76), with co-expression of the IL-5 transgene. The cytokines IL-4 and IL-13 and the STAT6 PD-L1 inhibitor signalling pathway through which they work are important for eosinophil recruitment into the skin following N. brasiliensis infection and most importantly, deletion of these genes or the IL-4Rα chain gene, results in higher lung larval burdens during secondary infections (76). IL-4, IL-13 and STAT6 had previously been shown to be important for resistance
at the level of the gut, with gene deletion delaying the clearance of intestinal larvae and adult worms in primary infections (72,85). Our recent findings have now highlighted the importance of these cytokines Protein Tyrosine Kinase inhibitor for early resistance to larvae and this may be a critical result when developing vaccines for helminths such as the hookworms, S. stercoralis and Schistosoma, which enter the host via the skin. In addition to facilitating the recruitment of eosinophils, complement also mediates attachment to N. brasiliensis larvae in vitro and in vivo (78,79). C3 can be detected on infectious-stage larvae incubated with sera from WT, C1qa−/−
and C4−/− mice and these sera facilitate the adherence Niclosamide of eosinophil-rich leucocyte populations (78). In contrast, C3 cannot be detected on L3 incubated with sera from factor B−/− and C3−/− mice, and leucocyte adherence is inhibited in this context. Infective-stage larvae activate murine complement via the alternative pathway, but lung-stage (L4) larvae also activate complement via the lectin pathway (78). Endogenously derived C3 products are readily detectable on larvae recovered from the skin within 30 min of injection, but are found at much lower levels by 150 min pi. Leucocyte adherence to 24- and 48-h lung larvae is also minimal, even when an exogenous source of complement is provided (78). Collectively, these data suggest that late-stage skin and lung-stage larvae upregulate expression of an
inhibitor of complement deposition or a factor capable of rapidly degrading C3, and this may inhibit leucocyte recruitment and adherence to larvae in the lungs up to 48 h pi. Within 30–150 min of injection into skin air pouches, larvae aggregate into very large clumps, and this is largely dependent on the alternative pathway of complement activation (75). Whilst it is difficult to mechanically dissociate these clumps in vitro (75), clearly 80-90% of larvae can escape from the skin during the first few hours of infection in a susceptible WT host (65). In contrast, in IL-5 Tg hosts larvae can be trapped in the skin for up to 24 h and are usually surrounded by a strong inflammatory infiltrate in which eosinophils predominate (65).
1A and B and D–F). The stimulatory effects of PstS1 were specific for memory cells since no proliferative response or cytokine release was www.selleckchem.com/products/FK-506-(Tacrolimus).html observed in spleen cells of naïve mice cultured with PstS1 (Fig. 1A and B and D–F). Moreover, PstS1 was also effective in stimulating memory T cells specific for other types of mycobacterial and nonmycobacterial antigens.
Indeed, PstS1 in vitro stimulation induced IFN-γ and IL-17 release by Ag85A specific (Fig. 2A) and by tetanus toxoid (TT) specific (Fig. 2B) memory T cells. DCs are central cellular mediators for priming and for memory T-cell activation. To evaluate whether the effects of PstS1 on Ag85B-specific memory T-cell activation were mediated through the stimulation of DCs, splenic DCs from naïve mice were pulsed in vitro with Ag85B, PstS1, or combination of proteins and then used as stimulators of spleen cells from Ag85B- or PstS1-immunized mice. Activation of Ag85B-specific memory T-cell proliferation was observed upon stimulation with DCs pulsed with Ag85B, PstS1, or the combination of proteins (Fig. 3A). In contrast, PstS1-specific memory T cells proliferated only in response to PstS1-pulsed, but not Ag85B-pulsed DCs (Fig. 3A). In addition, PstS1-pulsed DCs were able to induce release of IFN-γ and IL-17 by spleen cells of Ag85B-immunized mice (Fig. 3B–C). Ag85B memory T cells released even greater amounts of IL-22 in response
to PstS1-pulsed Depsipeptide mw DCs compared with Ag85B-pulsed DCs (Fig. 3D). A clear-cut additive effect on IFN-γ, IL-17, and IL-22 production was observed when DCs loaded with both proteins were used as stimulators (Fig. 3B–D). Similar cytokine responses were observed when sorted CD4+ T cells from Ag85B-immunized
mice were used as responders (Fig. 3E). The PstS1-mediated activation of Ag85B-specific splenocytes was not due to potential LPS contamination (Supporting Information Fig. 1A and B). Of note, Ag85B-pulsed DCs were able to stimulate IL-17 secretion by Ag85B-specific spleen (Fig. 3C) or CD4+ T (Fig. 3E) cells, in contrast with the undetectable IL-17 levels found in unfractionated Ag85B-specific spleen cells restimulated with Ag85B (Fig. 1E). This finding may suggest that the differentiation of Ag85B-specific Th17 cells has selective requirements for DC-derived Non-specific serine/threonine protein kinase signals, as reported elsewhere . Cytokine production by PstS1-specific memory T cells was observed only in response to DCs loaded with the related Ag (Fig. 3B–D). We next tested the potential of PstS1 to stimulate DC activities. PstS1, but not Ag85B, stimulation of splenic DCs induced upregulation of CD40, CD86, and MHC class II expression (Fig. 4A). According to their more activated phenotype, PstS1-treated DCs exhibited increased stimulatory capacity in a mixed leukocyte reaction of either CD4+ or CD8+ T cells from allogeneic mice, revealed by CFSE dilution, as compared with Ag-85B-treated DCs (Fig. 4B).