Another possible source of between-subjects variability

may be neuromaturation related to motor performance (Gesell, 1946). For example, bimanual coordination is dependent on the development of the supplementary motor area of the left and right frontal cortices and their interconnection through the corpus callosum (Diamond, 1991; Muetzel et al., 2008). A recent examination of 1-year-old infants with agenesis of the corpus callosum revealed significantly limited or delayed bimanual activity compared with typically developing children (Sacco, Moutard, & Fagard, 2006). Moreover, overflow movements, or limb movements ABT-888 datasheet that are extraneous to the primary motor action, diminish as the corpus callosum matures (Soska, Galeon, & Adolph, 2012), suggesting more efficient interhemispheric processing relevant for bimanual coordination. Because of the numerous, varied neural pathways influencing cortical structures, little else is known about the full role the corpus callosum plays in bimanual activity, but a promising direction

for this work would take into account the multiple influences on infants’ reaching pattern preferences to provide a systemic account of the developmental trajectory. The discrepancy between the session-to-session developmental trajectory that was depicted when reaching preference was averaged over all participants vs. when it was examined individually is noteworthy.

While most participants did show fluctuations between uni- and bimanual reaching preferences, the ANOVA alone did not Peptide 17 datasheet accurately reflect what several of the 25 participants actually experienced. By examining the three preference profiles revealed by the cluster analysis and the individual reaching trajectories relative to changes in other motor skill, we were able to avoid the pitfalls of using age as an explanatory variable (Adolph & Berger, 2006). The design of the present study allowed us to depict between-subjects differences and at the same time capture fluctuations in within-subject developmental trajectories. In so doing, we managed to avoid the drawbacks of averaging across a group without also examining the variability Fossariinae and were able to investigate developmental processes within a more accurate developmental framework of theory and design (van Geert & van Dijk, 2002; Lampl, Johnson, & Frongillo, 2001; Siegler, 2006). Our primary predictor of reaching preference was experience with a new locomotor skill, which did a moderately good job of predicting the decrease in bimanual reaching preference at the individual level. Future studies should delve even deeper into individual differences in motor ability and capture proficiency, which would be a better indicator of level of effort than experience alone.

The results also showed that the proliferation of B6 spleen cells with IL-2 pre-incubation was significantly weaker than that of the controls

without IL-2 pre-incubation (P = 0·0025, Fig. 2b). SOCS-3 can inhibit the Th1-type polarization which plays a critical role in the pathophysiology of aGVHD [21,22,35,36]; therefore, we explored whether high SOCS-3 mRNA expression induced by IL-2 pre-incubation can inhibit Th1-type polarization in B6 naive CD4+ lymphocytes. According to the regularity of expression of SOCS-3 mRNA, we pre-incubated B6 naive CD4+ lymphocytes and B6 spleen cells, respectively, with IL-2 for 4 h before stimulation of allogeneic antigen-BALB/c spleen cells inactivated by mitomycin for 48 h. We then collected the supernatants to detect the levels of IFN-γ and IL-4. The results showed that expression of IFN-γ and find more IL-4 of B6 naive CD4+ lymphocytes was different between pre-incubation of the two groups with or without IL-2. The IFN-γ level in group pre-incubation with IL-2 was lower than that in group pre-incubation without IL-2 (P = 0·000, Fig. 3a). The IL-4 level in group pre-incubation with IL-2 was higher than that in group pre-incubation without IL-2 (P = 0·000, Fig. 3a). The expression selleckchem of IFN-γ and IL-4 of B6 spleen cells was similar to that of B6 naive CD4+ lymphocytes (P = 0·002, and 0·000, respectively, Fig. 3b) We assessed suppressive function in vivo in an aGVHD mice model.

We used female BALB/C recipients and male B6 donors. All recipients received 5 Gy TBI as conditioning regimen. In group A (n = 9), B6 spleen cells (3 × 107 cells) were injected intraperitoneally into recipients as control. We first explored whether aGVHD was inhibited in the recipients (group B, n = 9) which received Rutecarpine 3 × 107 B6 spleen cells pre-incubated with IL-2 before intraperitoneal injection. We found that the mean survival time of group B (14·4 ± 1·5 days) was not statistically different from that of group A (12·2 ± 3·1 days) (P = 0·3090, Fig. 4a). The scores of aGVHD symptoms between the two groups were

also not different (P = 0·7851). These findings suggest that IL-2 pre-incubation can up-regulate the expression of SOCS-3, but it was a short-lived gene product induced by IL-2 in lymphocytes. If the spleen cells with short-lived SOCS-3 did not receive allogeneic antigen in time, aGVHD could also not be inhibited; therefore, we projected another group (group D, n = 9) in which recipients received 3 × 107 B6 spleen cells which were presented with host-allogeneic antigen-inactivated BALB/C spleen cells for 72 h after IL-2 pre-incubation for 4 h. The results showed that aGVHD was inhibited significantly in group D. The mean survival time of group D was 44·1 ± 23·8 days, which was longer than that of group A (P = 0·0042, Fig. 4b). The score of aGVHD in group D was lower than that in group A (P = 0·0046).

The recombinase activating genes (RAG) are essential for NVP-BGJ398 editing and revision of the antigen receptors. The overall purpose of these processes lies in diversifying the antigen receptor repertoire and in revising autoreactive receptors to prevent autoimmunity. Consequently, these enzymes become promoters of self-tolerance during lymphocyte differentiation.

Once T and B cells mature, RAG expression is turned off and the cells are released to the periphery. However, re-expression of RAG proteins and receptor revision have been reported in mature peripheral blood B cells from patients with autoimmune diseases such as systemic lupus erythematosus (SLE) and juvenile idiopathic arthritis.[1-4] In these studies re-expression of RAG correlated with CD5 expression and was found to be dependent on interleukin-6 (IL-6).[5-7] Albeit RAG re-expression in the autoimmune context may result

from abnormal B-cell activation, the molecular mechanisms enabling re-expression and consecutive rearrangement processes remain to be investigated. Important evidence for a role of Toll-like receptors (TLR) in B-cell-mediated disease comes from studies dealing with autoimmune disorders. In this context, a central role of TLR was demonstrated in promoting the expansion of autoreactive B cells and autoantibody production.[8-10] Moreover, patients with SLE display an elevated frequency of TLR9-expressing B cells[11, 12] and TLR9-reactive CD27– effector memory B cells.[13] Vildagliptin selleck compound Nonetheless, it was also reported that TLR9 exerts tolerogenic effects in murine SLE[14] and that patients with defective TLR signalling display elevated frequencies of autoreactive B-cell receptors (BCR),[15] indicating that TLR might influence receptor editing. However, only recently a clinical trial using TLR9 agonists, e.g. phosphorothioate-modified CpG oligodeoxynucleotides (CpGPTO) as adjuvant was halted because severe autoimmune disease developed in one subject.[16]

This unexplained incident encouraged us to investigate the role of TLR9 in B-cell tolerance, i.e. its role in receptor revision. The use of human materials was approved by the local ethics committee and written consent was obtained from donors. Total B cells were isolated from peripheral blood mononuclear cells with anti-CD19 microbeads (Miltenyi Biotec, Bergisch-Gladbach, Germany) (purity 98·5 ± 1%). For Igκ+ B-cell purification Igλ+ B cells were depleted with anti-Igλ-phycoerythrin (PE) and anti-PE microbeads before selection of Igκ+ B cells with anti-CD19 microbeads (purity 99 ± 0·5%). IgM+, IgM−, CD27+ and CD27− B-cell fractions were isolated as described previously.[17] Plasmacytoid dendritic cells were isolated with anti-BDCA4 beads (Miltenyi Biotec). Culture medium contained 5–10% heat-inactivated autologous serum [or 10% fetal calf serum (FCS; Biochrom, Cambridge, UK) for immunoglobulin assays]. Thymus was homogenized in Trizol (Invitrogen, Karlsuhe, Germany) or RIPA buffer.

Fifty-eight per cent of DS

children and 13% of non-DS children met criteria for acute lung injury. Similarly, 46% of DS children and 7% of non-DS children were diagnosed with acute respiratory distress syndrome (ARDS). None of the DS children in this cohort with acute lung injury died, whereas others have reported a mortality rate of about 5% of non-DS children with ARDS. These data suggest that children with DS have an increased risk of progressing towards ARDS, although with low mortality, and support the hypothesis of www.selleckchem.com/products/Neratinib(HKI-272).html abnormal regulatory mechanisms of inflammation, such as an imbalance of anti-oxidants and oxidative stress [19], which might lead to apoptosis in lung tissue. A review of a large cohort of DS children in Sweden and Denmark [20] revealed a 12-times increased risk for mortality due to infections, especially septicaemia. This excess of mortality was consistent with data from a recent study in which DS children showed a 30% higher risk of fatality secondary to sepsis when compared to other children hospitalized for sepsis [21], after controlling for confounding factors including pathogens and co-morbid conditions. The above studies highlight the increased frequency and severity of respiratory tract

infections Selleckchem Gefitinib in DS children. These are predominantly ear infections; however, pneumonias occur frequently in children younger than 5 years of age and are likely to require hospitalization. Lung disease might be of more prolonged duration and might progress to ARDS. In addition to respiratory tract infections, periodontal disease is another condition of infectious aetiology that occurs frequently between

58% and 96% of individuals with DS [22]. Due to the complexity of the pathophysiology of gingivitis, the contributions of potential determinant factors such as abnormal immunity and poor oral hygiene have not yet been defined clearly. Defects in immunological parameters in DS have been described and postulated as explanations for the increased severity of infections RANTES seen in DS children [9,10]. Most of these infections are of the respiratory tract, suggesting abnormalities of the humoral immunity. However, differences in several compartments of the immune response have been reported [23–25] (Table 1). Reduced ranges of the different lymphocyte subsets were found to be of most significance in childhood, with subsequent improvement over age. T and B cell subsets are decreased below the 10th percentile of normal in almost 90% of DS children, and below the 5th percentile of normal in 60% of them. The normal early T cell expansion in infancy was not observed. Their thymus size was reported to be smaller than non-DS children, with decreased T cell percentages bearing the T cell receptor (TCR)-αβ and relatively reduced naive T cell percentages [26–28], resulting in mild to moderate lymphopenia.

The ability of the DNA vaccine constructs to elicit cellular immune responses makes them an attractive weapon as a safer vaccine candidate for preventive and therapeutic applications against tuberculosis. Tuberculosis (TB) is a major local, regional and global infectious disease problem with about 9 million new cases and

2 million deaths every year [1]. Mycobacterium tuberculosis kills more adults each year than any other single pathogen. The vaccination with Mycobacterium bovis bacille Calmette Guerin (BCG) is considered to be the most important tool to protect against TB [2]. In spite of its widespread use and many advantages like being inexpensive, safe at birth, given as a single shot and provision of some protection against leprosy, BCG vaccination remains controversial [2–4]. Target Selective Inhibitor Library The protection afforded by BCG vaccination has shown wide variations in different parts of the world, and its impact on the global problem of TB remains unclear [5]. Estimates of protection given by BCG against pulmonary TB vary greatly [4]. For example, a trial in British school children, in 1952, showed about 80% efficacy, whereas the Chingleput trial in India showed zero efficacy

of protection against adult pulmonary Trichostatin A cost TB, after BCG vaccination [4, 6]. This variability has been attributed to various factors including strain variation in BCG preparations, environmental influences such as sunlight exposure, poor cold-chain maintenance, genetic or nutritional differences between populations and exposure 4��8C to environmental mycobacterial infections etc. [5]. In addition, because of sharing most of the antigens, BCG vaccination induces a delayed-type hypersensitivity skin response to the purified protein derivative of M. tuberculosis (the stimulus used to test the individuals for tuberculous infection), which cannot be distinguished from exposure to M. tuberculosis [7]. This makes the use

of tuberculin skin test difficult for diagnostic or epidemiological purposes. Furthermore, BCG vaccination cannot be used in all groups of people, e.g. WHO has recommended that children with symptoms of HIV or AIDS should receive all the vaccines except BCG. This is because BCG is a live attenuated vaccine that might cause disease in immuno-compromised people rather than giving immunity [8]. Thus, there is an urgent need to develop M. tuberculosis-specific and safer vaccines against TB [6, 9]. The development of a better BCG vaccine or alternative vaccines needs the identification and evaluation of antigens recognized by protective immune responses [9]. In previous studies, we have identified RD1 PE35 (Rv3872), PPE68 (Rv3873), EsxA (Rv3874), EsxB (Rv3875) and RD9 EsxV (Rv3619c) as M. tuberculosis-specific antigens [10–13]. Furthermore, in vitro studies in patients with TB and healthy subjects infected with M. tuberculosis have shown that these antigens induced cellular immune responses that correlate with protection [9].

Among them apolipoprotein B-100, complement component 3, etc decreased in the last, indicating the association with nephrotic condition. On the other hand, complement component 9, apoprotein E increased probably suggesting of the association with clinical remission. Of interest is that apolipoprotein Staurosporine E and serum amyloid P were high in both the first and last sessions. Moreover, serum apolipoprotein

E was also high in a non-responder group. Conclusion: The present proteomic analysis revealed that the increase in serum apolipoprotein E may predict the responsiveness of LDL-A in steroid-resistant nephrotic syndrome. Further study may clarify the more detailed mechanism of the LDL-A in an intractable setting of steroid-restant nephrotic syndrome. JEONG KYUNGHWAN1,2, ASANUMA KATSUHIKO2,3, LYDIA AIDA4, TAKAKI MIYUKI2, ASAO RIN2, KODAMA Roxadustat FUMIKO2, ASANUMA ETSUKO2, TOMINO YASUHIKO2 1Division of Nephrology, Department of Internal Medicine, Kyung Hee University, Seoul, Korea; 2Division of Nephrology, Department of Internal Medicine,Juntendo University, Faculty of Medicine, Tokyo, Japan; 3Laboratory for Kidney Research, Medical Innovation Center, Graduate School of Medicine, Kyoto University, Kyoto, Japan; 4Division of Nephrology and Hypertension,

Department of Internal Medicine, Cipto Mangun Kusumo Hospital, University of Indonesia, Jakarta, Indonesia Introduction: Blockade of the renin-angiotensin system plays a key role in suppressing the progression of renal diseases. It has been well unknown whether this therapy provides additional effects when combined with vitamin D or its analog in an adriamycin (ADR)-induced nephropathy model. Methods: Here we evaluated the effect of applying the combination of an AT1 receptor blocker, telmisaltan, and a vitamin D analog, oxacalcitriol, in ADR-induced nephropathy mice and immortalized murine podocytes. Podocyte injury was assessed by podocyte apoptosis using the TUNEL assay, podocyte counting, and podocyte-specific expressed protein by immunofluorescence and

western blot analysis. Results: Mice with ADR-induced nephropathy (9.5 mg/kg single intravenous injection) developed progressive albuminuria and glomerulosclerosis within 30 days, accompanied by decreased expression of slit diaphragm-associated proteins (nephrin and podocin), reduced numbers of Sclareol podocytes, and increased systolic blood pressure. Treatment with telmisartan (0.1 mg/kg ip injection, everyday) or oxacalcitriol (0.05 μg/Kg ip injection, three times per week) alone moderately ameliorated the kidney injury; the combined treatment most effectively reduced the albuminuria and glomerulosclerosis. These effects were accompanied by restoration of slit diaphragm-associated proteins (nephrin and podocin) and podocyte apoptosis and podocyte loss in the glomeruli. Cultured podocytes were exposed to 0.25 μg/ml of ADR with telmisartan (10−7 M) or oxacalcitriol (10−8 M) and combination.

Isotype-matched control antibodies were used for assessment of background fluorescence. Multiple simultaneous cytokine detection for IL-2, IL-4, IL-6, IL-10, IL-17a, tumour necrosis factor (TNF)-α and interferon (IFN)-γ was performed using the human T helper type 1 (Th1)/Th2/Th17 cytokine kit (BD Biosciences) on a MACS QuantTM analyser and MACS Quantify version 2.1 software (Miltenyi Biotec) as well as the FCAP Array software, version 1.0.1

(BD Biosciences). The assays were performed with undiluted supernatants and with supernatants diluted to 1:10 with PBS (Invitrogen). In addition, enzyme-linked immunosorbent assays buy Lapatinib (ELISA, n = 5 per group) were performed with commercial kits for detection of IL-1ra (BioSource Europe

SA, Nivelles, Belgium) and IL-1β and IL-8 (Invitrogen Corporation, Camarillo, CA, USA), according to the manufacturers’ protocols. Statistical analysis was performed using spss software (SPSS Inc., released 2009; PASW Statistics for Windows, version 18.0; SPSS Inc., Chicago, IL, USA). One-way analyses of variance (anova) followed by Bonferroni adjustment were performed to compare the different groups of lymphocyte cultures after creating interindividual differences for each patient. Differences were considered statistically significant for P-values smaller 0·05. Results are shown as Selleck NSC 683864 means ± standard deviation (s.d.). An important variation could be observed of Treg percentages after magnetic separation (Fig. 1a). Because of the donor-associated varying baseline

Treg percentages before co-culture, intraindividual differences between the Treg percentages after single- and co-cultures at day 5 and the initial Treg http://www.selleck.co.jp/products/BIBW2992.html percentage (day 0) were calculated in each group. There were no significant differences in CD4 expression (P = 0·522 between the groups) and in the percentages of CD4+CD25+ cells (P = 0·258) between the groups. Tregs were defined as CD4+CD25+CD127– or CD4+CD25+FoxP3 cells, respectively. The gating strategy is demonstrated in Fig. 1b. There was a negative correlation between CD127 and FoxP3 expression, the mean intraindividual difference between CD127– and FoxP3+ cells being 4·62 ± 6·31%. Both B-MSC– and S-MSC–lymphocyte co-cultures showed no significant changes in the Treg proportion, while we observed a significant decrease in the proportion of Treg in T cell monoculture (Fig. 2). This was the case for CD4+CD25+CD127– cells (Fig. 2a, P < 0·001 for both T cell single-culture versus B-MSC/T cell co-culture and S-MSC/T cell co-culture) and CD4+FoxP3+ cells (Fig. 2b, P = 0·006 for T cell single-culture versus B-MSC/T cell and P = 0·005 versus S-MSC/T cell co-cultures). There were no statistical differences between S-MSC/T cell and B-MSC/T cell co-cultures regarding CD127 and FoxP3 expression. The MSC effect on Treg-enriched CD4+ lymphocyte culture was independent of the T cell : MSC ratio (Fig. 2c).

55 In addition, the number of HLA-DR+ cells

noted in urine sediments of AR patients is approximately sixfold higher than those with stable graft function and the HLA-DR+ cell counts correlate with Banff score.56 Extending these immunohistochemical findings to non-invasive assessment, we have reported that soluble HLA-DR was increased in the urine of AR patients by ELISA.57 Sigdel et al., in a comprehensive proteomic analysis of AR urine sample towards stable graft function and healthy controls, reported nine proteins Roxadustat in vitro specific for AR.13 Four out of nine of these proteins were HLA class II-related proteins.13 Elevated levels of soluble HLA-DR is detectable in urine up to 5 days prior to kidney rejection symptoms, providing a specificity of 98% and sensitivity of 80% for prediction of AR.57 HLA-DR identified in the urine of AR transplant patients was partially truncated and not exosome-associated, suggesting it is either a result of alternative mRNA splicing or a product of proteolysis. The combination of inflammatory biomarkers together with other urinary tubular biomarkers reflecting cell regeneration ability, such as KIM-1 and NGAL, may provide a valuable biomarker panel to indicate different

states or inflammation or regeneration. There is a long history of interest in the urine as source of biomarkers given its ease selleck of collection at the bedside, or in the outpatient setting. Recent advancements in modern technologies like RNA or DNA microarray and proteomics have further unravelled potential biomarkers for AR.5,58,59 An ideal biomarker should: (i) allow early detection of renal injury while identifying the nephron segment most affected; and (ii) provide a quick and reliable measurement by a cost-efficient colorimetric-based assay or urine dip stick test. The above TEC biomarkers have shown promise in both human and animal studies to associate specifically

to TEC injury and can be measured by ELISA (Table 1). Ergoloid However, AR is associated with multiple causes and various medical problems and even treatments (e.g. nephrotoxicity). It is unlikely that a single biomarker will provide sufficient sensitivity and specificity enough to cover the full spectrum of AR for clinical assessment. Combining biomarkers to include markers of TEC damage and cellular infiltration, such as FOXP3, CD103 and Granzyme B, may further improve the specificity and sensitivity of biomarker testing.60 For example, increased mRNA levels of FOXP3, perforin and Granzyme B were reported in both urine and peripheral blood samples of patients during AR.5,61–63 A combination of FOXP3 mRNA and creatinine predicted the resolution of AR with 90% sensitivity and 96% specificity, better than the individual biomarkers when tested alone.

To study cross-presentation, the LyUV-treated LCMV-infected HEK cells (5×105 cells/well) were prepared for the assay as described previously 7. Where indicated, inhibitors were added to the APC 45 min before adding the ADC and maintained during the incubation periods. In certain experiments, RNase treatment of ADC was performed. ADC were lysed and treated with 10 μg/mL of RNase for 20 min at RT followed by two washing steps before UVB treatment. AZD9668 ic50 To test for cross-priming, B6 mice were injected i.p. with HEK293 (negative control) or LCMV-infected

HEK cells (7×106) treated as LyUV. After 7 days, splenocytes were obtained and stained with 0.5–1 μg of PE-labeled tetramers 36 as described previously 37. Alternatively, epitope-specific CTL were expanded in vitro before performing ICS assays as described previously 7. For ex vivo antigen presentation, peritoneal cells were collected 8 h later using PBS (10 mL). Positive selection for CD11c+ from peritoneal exudates was carried out with a mouse CD11c+ immunomagnetic selection kit from EasySep® (Vancouver, this website BC, Canada). CD11c+ and CD11c− cells were coincubated

with peptide-specific CTL at a ratio of 3:1 for 3 h in the presence of BFA (10 μg/mL) and ICS was performed as described above. Statistics were performed using the paired, two-tailed t-tests 3-mercaptopyruvate sulfurtransferase and differences in results between treatment conditions were deemed significant when p<0.05. The authors thank Dr. Groettrup, Dr. van den Broek, Dr. Zinkernagel, Dr. Rock and the NIH tetramer facility for providing reagents, and grants from NSERC to S. B., CIHR to A. L., and LG Fellowship to A. A. Conflict of interest: The authors declare no financial or commercial conflict of interest. "
“Although notable progress has been made in the therapeutic management of patients with chronic kidney

disease in both conservative and renal replacement treatments (dialysis and transplantation), the occurrence of medication-related problems (lack of efficacy, adverse drug reactions) still represents a key clinical issue. Recent evidence suggests that adverse drug reactions are major causes of death and hospital admission in Europe and the United States. The reasons for these conditions are represented by environmental/non-genetic and genetic factors responsible for the great inter-patient variability in drugs metabolism, disposition and therapeutic targets. Over the years several genetic settings have been linked, using pharmacogenetic approaches, to the effects and toxicity of many agents used in clinical nephrology. However, these strategies, analysing single gene or candidate pathways, do not represent the gold standard, being the overall pharmacological effects of medications and not typically monogenic traits.

Our model makes use of selective in-vivo expression of individual MHC II alleles on a C57BL/6 (IAb IEneg) background, which reconstitute IEdb expression and thereby allow presentation of moth cytochrome c (MCC) to the 5C.C7 TCR. Using host mice transgenic for the MHC II IE alpha chain, we have restricted expression PD0325901 cell line of IE to radioresistant LCs, while maintaining normal T cell homeostasis

via expression of IAb on all host and donor-derived DCs. We have demonstrated that LCs, as the sole antigen-presenting subset in this model, induce deletion of CD4+ T cells even when highly activated by exposure to multiple TLR and inflammasome-mediated signals. Thus our results indicate that LCs are precommitted to the induction of immunological tolerance. LCs can also inhibit the immune response driven by radiosensitive, immunogenic DC subsets. The use of this model has thus allowed the first direct investigation of the in-vivo function of this website LCs, in contrast to the essentially indirect ablation studies in which the function of multiple DC subsets is assessed in the presence or absence of LCs [8]. While chimeric models are useful for assessing the function of LCs, restricting

functional presentation capacity to defined DC subsets in tissues such as gut and lung remains a challenge. The development of further transgenic and knock-in models that will allow functional analysis of individual DC subsets in mice possessing the full complement of MHC-expressing DCs

remains a high priority. The goal of DC subset biology, in the context of T cell responses, is to understand how DCs control the many classes of immune responses that are generated in vivo. Defining the individual functions of DC subsets should allow us to develop a more complete understanding of the mechanisms controlling T cell-mediated immunity and tolerance, maximizing the therapeutic potential of targeting DC subsets for future translation into the clinic. The recent demonstration that mouse and human DC subsets are related much Decitabine more closely than previously believed underlines the importance of studying DC biology in the mouse using physiological models. The limitations in the models currently available to study DC subset control of T cell responses (summarized in Table 2) highlight the importance of careful interpretation of the results from these models. The improvement and combination of current models should allow for a clearer picture of DC biology. The authors have no competing interests. “
“Conditional ligands have enabled the high-throughput production of human leukocyte antigen (HLA) libraries that present defined peptides. Immunomonitoring platforms typically concentrate on restriction elements associated with European ancestry, and such tools are scarce for Asian HLA variants.