Onychomycosis is a fungal infection of the nails, caused by dermatophytes,

yeast and moulds. In this study, 228 patients with psoriasis aged between 18 and 72 were examined (48 – from Plovdiv, Bulgaria; 145 – from Pleven, Bulgaria and 35 – from Thessaloniki, Greece); 145 of them were male and 83 of them were female. The examination of the nail material was performed Ku-0059436 concentration via direct microscopy with 20% KOH and nail samples plated out on Sabouraud agar methodology. The severity of the nail disorders was determined according to the Nail Psoriasis Severity Index (NAPSI). Positive mycological cultures were obtained from 62% of the patients with psoriasis (52%– Plovdiv, Bulgaria; 70%– Pleven, Bulgaria and 43%– Thessaloniki, Greece). In 67% of the cases, the infection was caused by dermatophytes, in 24% by yeast, in 6% by Luminespib purchase moulds and in 3% by a combination of causes. All patients with psoriasis were identified with high levels of NAPSI, whereas the ones with isolated Candida had even higher levels. Seventeen percentage of the patients have been treated with methotrexate, 6% have been diagnosed with diabetes and 22% have been reported with onychomycosis and tinea pedis within the family. An increased

prevalence of onychomycosis among the patients with psoriasis was found. Dystrophic nails in psoriasis patients are more predisposed to fungal infections. The mycological examination of all psoriasis patients with nail deformations is considered obligatory because of the great number of psoriasis patients diagnosed with onychomycosis. Isotretinoin “
“Pyomyositis is an infection of skeletal muscle that, by definition,

arises intramuscularly rather than secondarily from adjacent infection. It is usually associated with bacterial infection, particularly Staphylcococcus aureus. Fungi are rare causes, and Blastomyces dermatitidis has not been reported previously. In this case series, we report two cases of pyomyositis caused by B. dermatitidis. Cases were prospectively identified through routine clinical care at a single academic referral hospital. Two patients with complaints of muscle pain and subacute cough were treated at our hospital in 2007. Both patients were found to have pyomyositis caused by B. dermatitidis– in the quadriceps muscles in one patient, and in the calf muscle in another – by radiological imaging and fungal culture. Both were also diagnosed with pneumonia caused by B. dermatitidis (presumptive in one, confirmed in the other). There was no evidence of infection of adjacent structures, suggesting that the route of infection was likely direct haematogenous seeding of the muscle. A review of the literature confirmed that although B. dermatitidis has been described as causing axial muscle infection secondary to adjacent infection such as vertebral osteomyelitis, our description of isolated muscle involvement (classic pyomyositis) caused by B.

Haller, University of Freiburg, Freiburg, Germany), human α-defensins, or isotype control. Three selective areas of oral epithelium: upper, middle, and lower parts of each tissue specimen were counted for MxA positive cells. The immunoreactivity of MxA staining was given a semiquantitative score ranging from score 1–3. Score 1 = the area of positive cells was less than 10% in the counting field, score 2 = 10–50%, and score 3 = more than 50%. Nontoxic concentrations of different antimicrobial peptides

for HGECs were predetermined as assessed by cell viability (MTT assay and Trypan blue exclusion). HGECs, normal human bronchial epithelial cells (Clonetics) Selleck Doxorubicin and primary human microvascular endothelial cells (Clonetics) were treated with nontoxic doses of either α-defensin-1 (10 μM); α-defensin-2 (10 μM); α-defensin-3 (10 μM); β-defensin-1 (10 μM); β-defensin-2 (10 μM); β-defensin-3 (0.5 μM); LL-37 (2 μg/mL); or IFN-α (100 U/mL). After 6 h of treatment with antimicrobial peptide or cytokine, mRNA expression of MxA was analyzed.

In neutralization buy Pirfenidone experiment, cells were treated with α-defensin-1 or IFN-α in the absence or presence of neutralizing antibodies against IFN-α (400 neutralization unit/mL) and IFN-β (400 neutralization unit/mL). After 24 h of treatment, immunohistochemical analysis of MxA protein was carried out. H5N1 virus (A/open-billed stork/Nahkonsawan/BBD0104F/04) was isolated from cloacal swabs of live Asian open-billed storks between 2004–2005 and propagated in Madin-Darby canine kidney cells using MEM (Gibco, Grand Island, NY, USA) supplemented with 10% FBS (Hyclone, Logan, UT, USA) and penicillin and streptomycin [[48]]. The sequence

data of the virus was submitted to GenBank with accession numbers DQ989958. The virus was grown in Madin-Darby canine kidney cells and the titer of virus stock was determined as described previously new [[48]]. All experiments with H5N1 virus were performed in a Biosafety Level 3 facility (Mahidol University) by trained researchers. HGECs (40,000 cells/well) were treated with either α-defensin-1 (10 μM); α-defensin-2 (10 μM); α-defensin-3 (10 μM); β-defensin-1 (10 μM); β-defensin-2 (10 μM); β-defensin-3 (0.5 μM); LL-37 (2 μg/mL); or IFN-α (100 U/mL) for 24 h. They were washed two times and then co-cultured with H5N1 virus at MOI 1 (1 PFU/cell). After 1 h, the inoculum virus was removed and the HGECs were washed two times with PBS and cultured with fresh medium. Virus titers in culture supernatants and cytopathic effect were determined 48 h postinfection. To assess the number of infectious particles (plaque titers) in cell culture supernatants, a plaque assay using Avicel (RC-591, FMC Biopolymer, Germany) was performed in 96-well plates [[49, 50]].

High-risk haematological malignancies included acute leukaemias, chronic myelocytic leukaemia with blastic transformation, myelodysplastic syndromes that required intensive chemotherapy and high-grade non-Hodgkin’s lymphomas. Patients who gave informed consent were included in the study starting from the day they were admitted to the wards and followed up until death, discharge or withdrawal of consent, whichever occurred earlier. Death or discharge within 10 days of hospitalisation, less than

10 days of neutropenia or major difficulty in obtaining blood samples were the exclusion criteria. Demographic characteristics, NVP-AUY922 cost underlying diseases and risk factors for invasive fungal infections (IFI), such as administration of chemotherapy, corticosteroids, antimicrobials, total parenteral nutrition within 30 days and stem-cell transplantation within 1 year, were noted. Patients were followed up by daily visits for vital signs, existing or newly developing signs and symptoms, clinical and laboratory findings. Colony stimulating factors, chemotherapeutic and antimicrobial agents administered were recorded during each visit. Culture growths and the results of the imaging studies were also noted. The MLN0128 purchase study protocol required that blood be drawn twice a week during the follow-up of the patients,

however because of the problems in venous access and reluctance of the patients, regular sampling could not be performed all the time. Blood samples were then transported to the laboratory and preserved at −70 °C until all the specimens were analysed by the ELISA method at the end of the study period. All patients with haematological malignancies who developed fever were consulted with the infectious diseases team as a routine part of patient care at our centre. GM levels were tested subsequently; therefore the primary physician and the infectious Adenosine diseases consultant were not aware of the results during patient care. No antifungal prophylaxis was used in this cohort of patients. Patients were treated with amphotericin B formulations

during inpatient periods and discharged on oral itraconazole when indicated for IA. Invasive fungal infections were defined according to the European Organization for Research and Treatment of Cancer – Mycoses Study Group (EORTC-MSG) consensus case definitions.27 As this study aimed to evaluate the accuracy of GM in diagnosis, GM positivity was not used as a microbiological criterion for classifying IA. Galactomannan levels were studied by sandwich ELISA commercial kit (Platelia®Aspergillus; Bio-Rad Laboratories) in accordance with the manufacturer’s instructions. Results are checked with positive and negative controls. The GM index was expressed as the ratio of the optical density of the sample relative to the optical density of the threshold control.

They analysed 12 cases of Aspergillus osteomyelitis (nine patients (75%) received surgical therapy) and found that survival was improved

by surgery (P = 0.05). In a recent publication, Gamaletsou reviewed 180 patients with Aspergillus osteomyelitis. Eighty (44%) followed a haematogenous mechanism, 58 (32%) contiguous infections and 42 (23%) direct inoculation. The most frequently infected sites were vertebrae (46%), cranium (23%), ribs (16%) and long bones (13%). Patients with vertebral Aspergillus osteomyelitis had more previous orthopaedic surgery (19% vs. 0%; P = 0.02), while those with cranial osteomyelitis had more diabetes mellitus (32% vs. 8%; P = 0.002) and prior head/neck surgery (12% vs. 0%; P = 0.02). buy Opaganib Radiologic findings included osteolysis, soft-tissue extension and uptake on T2-weighted images. Vertebral body Aspergillus osteomyelitis Epigenetics Compound Library was complicated by spinal-cord compression in 47% and neurological

deficits in 41%. Forty-four patients (24%) received only antifungal therapy, while 121 (67%) were managed with surgery and antifungal therapy. Overall mortality was 25%. Median duration of therapy was 90 days (range, 10–772 days). There were fewer relapses in patients managed with surgery plus antifungal therapy in comparison to those managed with antifungal therapy alone (8% vs. 30%; P = 0.006).[54] In the most recently published study by Gabrielli in 2014, 310 cases of Aspergillus osteomyelitis were reviewed, 193 (62%) were treated with a combination of an antifungal regimen and surgery, 80 (26%) were treated with an antifungal regimen alone and nine patients (3%) only received surgical treatment. An interesting result from this study was that significantly bigger proportion of patients with a favourable outcome underwent surgery (for trauma or fractures) prior to the infection (P = 0.002), which indicates

that a possible external Thymidylate synthase contamination leads to a better outcome than infections which develop due to dissemination in an immunocompromised host. Among the group of patients who received antifungal therapy, those who underwent surgery in addition did not have a better outcome than those who did not (P = 0.398). It has to be taken into consideration, however, that patients in the need for surgery might have had progressed Aspergillus infection, which may have been associated with a poorer outcome per se. Gabrielli also analysed cases from 1936 to 2013, the extend and methods of surgical interventions and therefore the indications for surgery have dramatically changed in that time period.[55, 56] Different results regarding the outcome of surgical therapy in Aspergillus osteomyelitis and joint infection were published by Koehler et al. [57] in 2014. In his review, 37 of 47 patients (74%) received combined surgical and antifungal treatment, which resulted in survival rates of 78% vs.

0001) (Fig. 2C). The establishment of functional T-cell memory is vital for the success of an immunization protocol. To assess if functional CTL responses could be generated by a single immunization or if a prime boost regime Selleck 5-Fluoracil were required, C57BL/6 mice were given single or multiple immunizations with TRP2/HepB human IgG1 DNA. No epitope-specific responses were detectable 20 days after a single immunization with TRP2/HepB human IgG1 DNA, but high-frequency responses were detectable after two immunizations (p=0.026) which increased further

with another immunization (p<0.0001) (Fig. 2D). The avidity of responses after two or three immunizations was analyzed. The responses induced in mice receiving two or three DNA immunizations were of high avidity (1.4×10−12 M and 1.8×10−12 M,

respectively). There is no significant difference in avidity between these two groups (p=0.89) (Fig. 2E). As both the frequency and avidity of the CTL response appear enhanced, the question “was avidity related to frequency?” arose. Over 80 mice were immunized with TRP2/HepB human IgG1 DNA and the frequency and avidity of responses measured. The avidity of the TRP2-specific responses ranged from 5×10−8 M to 5×10−13 M peptide. No significant correlation find more between avidity and frequency of TRP2 peptide-specific responses was identified, suggesting they are independent events (Fig. 3A). It is possible that xenogeneic human Fc influences the frequency and avidity of responses induced. Comparison of responses from immunization with human IgG1 or an equivalent murine IgG2a construct reveals similar frequency and avidity (Fig. 3B), suggesting that the xenogeneic human Fc was not influencing the response. Synthetic peptides have short half lives in vivo and are poor immunogens as they

have no ability to specifically target professional Ag presenting cells such as DC. Current therapies are showing DC pulsed with peptide induce an efficient immune response. TRP2/HepB human IgG1 DNA immunization was compared to DC pulsed with HepB/TRP-2 linked peptide. TRP2/HepB human IgG1 DNA demonstrated similar frequency responses compared to those Ribonucleotide reductase elicited by peptide-pulsed DC, both of which were superior to peptide immunization (p=0.0051 and p=0.0053) (Fig. 4A). Analysis of the avidity of responses reveals that the avidity in TRP2/HepB human IgG1 DNA immunized mice is 10-fold higher than with peptide-pulsed DC (p=0.01) (Fig. 4B). The TRP2 specific responses were analyzed for ability to kill the B16F10 melanoma cell line in vitro. Figure 4C shows that although responses from peptide and peptide-pulsed DC immunized mice demonstrate a good peptide-specific lysis, mice immunized with TRP2/HepB human IgG1 DNA showed better killing of the B16 melanoma cells (p=0.003). The enhancement of avidity could be related to direct presentation of the epitopes by the Ab–DNA vaccine and similar responses may be elicited by a DNA vaccine incorporating the native TRP2 Ag.

An internal standard is used to ensure precision in mass determination. The result is that the Ibis

universal biosensor detection system can identify the amplicons produced by a carefully designed primer set, with a high degree of accuracy that is stated as a percentage in the ‘read out’ data and with a sensitivity that detects all organisms present as >1% of the total microbial population in the sample. The system also detects and identifies fungi and viruses, and detects the presence of the bacterial genes that control resistance to antibiotics. Primer sets can be designed selleck screening library to focus on the pathogens usually seen in a particular medical situation, such as orthopedic infections, so that sensitivity and accuracy can be enhanced in the parts of the bacterial ‘tree of life’ (Fig. 5) in which the majority of the ‘usual suspects’ are located. The time required for DNA extraction is short, except in exceptional cases, and the PCR amplification process is rapid and automated, so that the Ibis system can detect and identify all of the bacteria present in a sample in <6 h, and biofilm cells are detected with the same sensitivity as planktonic cells. We have initiated prospective

double-blinded studies of both suspected infections of total joint prostheses, and of infected nonunions of the tibia/fibula following open trauma, in which we will compare data obtained from cultures with data generated using the Ibis system. Clinical decisions will be based on culture data because the Ibis system is not yet FDA approved, but after the code has been broken, BI 2536 order the sensitivity and accuracy of the Ibis system will be compared with that of cultures. In addition, the Ibis data will be considered retrospectively, as a potential basis for clinical decisions, in the light of clinical outcomes and in the light of additional evidence of the presence of bacterial biofilms, such as direct microscopic evidence using FISH probes. If Megestrol Acetate the sensitivity and accuracy of the Ibis system are seen to exceed those

of traditional cultures, we will support their adoption for the diagnosis of bacterial infections in all aspects of orthopedic surgery. “
“Here, we report on the successful programming of dendritic cells (DCs) using selectively applied mixtures of chemokines as a novel protocol for engineering vaccine efficiency. Antigen internalization by DCs is a pivotal step in antigen uptake/presentation for bridging innate and adaptive immunity and in exogenous gene delivery used in vaccine strategies. Contrary to most approaches to improve vaccine efficiency, active enhancement of antigen internalization by DCs as a vaccine strategy has been less studied because DCs naturally down-regulate antigen internalization upon maturation. Whereas chemokines are mainly known as signal proteins that induce leucocyte chemotaxis, very little research has been carried out to identify any additional effects of chemokines on DCs following maturation.

Moreover, combination therapy using cisplatin and human leucocyte antigen-A24-restricted human vascular endothelial growth factor receptor 1 (VEGFR1)-1084 and VEGFR2-169 in patients with advanced or recurrent adenocarcinoma of the stomach showed that the disease control rate (partial and stable disease) was 100% after two cycles of the combination therapy [25]. Delayed-type hypersensitivity response to leishmanial antigens has been widely used to assess the level of host protection to the disease [26]. It has been well established that induction of a DTH response is mediated via Th1 cell as it secretes IFN-γ which

is expressed during macrophage stimulation buy BAY 80-6946 for parasite killing [27]. The DTH responses to leishmanin were apparent during L. donovani infection in BALB/c mice as evident by an increase in the foot pad swelling after injection of leishmanin. The increase was much higher when the animals were treated with immunochemotherapy than the groups BAY 73-4506 nmr of animals treated with

chemotherapy or immunotherapy alone. This suggests that the mice treated with cisplatin + 78 kDa with or without adjuvant (MPL-A) developed a strong cell-mediated immune response indicating that drug treatment followed by vaccine therapy was helpful in reversal of immunosuppression caused by the parasite. Earlier studies from our laboratory reported an increased DTH response in animals treated with low dose of cisplatin [14]. Correlation between DTH responses and parasite load has also been reported [14, 15]. This was evident from our results where a strong positive correlation was observed between enhanced DTH response and reduced parasite load. The immunological response was further characterized by analysing the

distribution of IgG1 and IgG2a specific antibodies in the serum samples of infected and treated BALB/c mice. Production of IgG2a is normally associated with IFN-γ secretion and the development of a Th1 immune response. However, in contrast, production of the IgG1 is normally associated with IL-4 secretion and the development of Th2 type of response. The treated animals revealed higher IgG2a and lower IgG1 levels than the infected controls. However, maximum levels of IgG2a and minimum levels of IgG1 were observed in animals learn more treated with cisplatin + 78 kDa + MPL-A than those animals that are treated with cisplatin alone or 78 kDa/78 kDa + MPL-A alone. It has been shown earlier from our laboratory that immunization of mice with 78 kDa + MPL-A resulted in significant increase in IgG2a response [6]. Moreover, a significant reduction in specific antibody titres was observed after treatment with immunochemotherapy (Glucantime + Leish-110f/MPL-SE) in dogs suffering from canine leishmaniasis [18]. Th1 and Th2 cell lymphocytes are important mediators in generating immunity to leishmaniasis and can be distinguished by the cytokines they secrete.

Induction of in vitro Treg cells was most easily accomplished with anti-CD3 mAb mitogen-based stimulation. Therefore, to control for the use of mitogen-based stimulation, it was necessary to confirm that n-butyrate anergized mitogen-stimulated CD4+ T cells similarly to antigen-stimulated CD4+ T cells. Primary cultures of isolated C57BL/6 CD4+ T cells were stimulated with plate-bound anti-CD3 mAb and soluble

anti-CD28 mAb for 7 days in the presence or absence of n-butyrate. As seen in Fig. 1A, n-butyrate reduced proliferation of CD4+ T cells by approximately 95% in mitogen-stimulated primary cultures. To test whether n-butyrate induced unresponsiveness was retained after the removal of the HDAC inhibitor, the CD4+ T cells from the primary culture were re-stimulated in secondary cultures that did not contain n-butyrate. As shown in Fig. 1B, control CD4+ T cells IWR1 from the

primary cultures proliferated vigorously when re-stimulated in secondary cultures. In contrast, CD4+ T cells from the n-butyrate-treated primary cultures proliferated 83–91% less than untreated CD4+ T cells. The retention of proliferative unresponsiveness in the secondary cultures demonstrated that the CD4+ T cells from the n-butyrate-treated mitogen-stimulated primary cultures were anergic. Anergy in CD4+ T cells usually involves an inability to generate IL-2 in association with proliferative unresponsiveness. Consequently, IL-2 secretion Selleckchem Ribociclib by the CD4+ T cells was also examined to confirm the onset of anergy (Fig. 1C). CD4+ T cells from control primary cultures secreted IL-2 in secondary cultures stimulated with anti-CD3 mAb. In contrast, IL-2

secretion Montelukast Sodium was inhibited in CD4+ T cells from the n-butyrate-treated primary cultures. The anergic CD4+ T cells did not generate any additional IL-2 beyond the detected background levels in response to anti-CD3 mAb stimulation in the secondary cultures. The decreased IL-2 concentration within the anergic CD4+ T cell culture supernatants had no bearing upon proliferation in the n-butyrate-treated CD4+ T cells as seen in Fig. 1B. Taken together, the results in Fig. 1 revealed that n-butyrate induced anergy within mitogen-stimulated CD4+ T cells as determined through significant reduction of proliferation and IL-2 secretion. To determine if n-butyrate increased the percentage of FoxP3+ Treg cells in primary or secondary cultures, CD4+ T cells from transgenic FoxP3EGFP C57BL/6 mice were stimulated in primary cultures with or without n-butyrate. Natural Treg cells as determined by the presence of FoxP3EGFP comprised approximately 8% of isolated lymphoid CD4+ T cells (data not shown). TGF-β was added to additional primary cultures to generate FoxP3+ T cells as a positive control [21]. Percentages of FoxP3+ T cells were quantified daily over the course of 5 days (Fig. 2A). The percentage of CD4+FoxP3+ T cells increased only in the primary cultures stimulated in the presence of TGF-β, as shown on Day 4 in Fig.

However, the authors caution that the applicability of these findings is reduced because the reporting of each outcome was limited to one or two trials in the meta-analysis.12 There is little evidence that calcium supplementation alone is effective in maintaining bone mineral density or reducing bone fracture risk. In a double-blind randomized controlled trial, Torres et al. studied the effects of daily low dose (1500 mg)

calcium supplementation in the first year post-transplant compared with a combination of this treatment with vitamin D supplementation (0.5 µg every other day) for the first 3 months post-transplant. They found that the combination treatment was more effective at preserving bone mineral density at the hip.16 A similar finding Kinase Inhibitor Library price was reported by Uğur et al.17 who, in Atezolizumab a randomized trial, compared four treatments: daily supplementation of 3 g calcium and 0.5 µg calcitriol; 3 g calcium carbonate with 0.5 µg calcitriol and nasal calcitonin; 3 g calcium alone; and no treatment. They showed that calcitriol with daily calcium supplementation abates the usual decrease in bone mineral density, however, they were unable to show a significant improvement in bone mineral density, possibly

due to small sample size and short duration of follow-up. There are no published studies examining the potential role of diet per se in preventing and treating bone disease in adult kidney transplant recipients. Meta-analysis of randomized controlled show that any intervention (bisphopshate, vitamin D sterol or calcitonin) for bone disease in kidney

transplant recipients reduces the risk of fracture in this population. These agents have also been shown to provide a statistically significant improvement in bone mineral density when given after transplantation, however, the clinical significance of this difference remains uncertain. There is little 3-mercaptopyruvate sulfurtransferase evidence that calcium supplementation alone is effective in maintaining bone mineral density or reducing bone fracture risk. Kidney Disease Outcomes Quality Initiative:18 No guideline on nutritional management including vitamin D or calcium. Recommendations regarding monitoring of serum calcium, phosphorus and intact parathyroid hormone. UK Renal Association: No recommendation. Canadian Society of Nephrology: No recommendation. European Best Practice Guidelines:19 Recommendations include: 0.25–0.5 µg/day calcitriol or 600 IU cholecalciferol; 1000 mg/day calcium (1500 mg post-menopause); treat persistent severe hypophosphatemia and hypomagnesaemia; cessation of smoking; and initiation of exercise. International Guidelines:20 Minimum calcium intake 1500 mg.

2D). Importantly, all vaccinated mice rapidly lost weight and succumbed to LCMV infection while nonvaccinated mice exhibited less weight loss and survived (Fig. 2E and F). In order to further decrease the number of memory CD8+ T cells we performed adoptive transfer of different numbers of NP118-specific memory CD8+ T cells (ranging from 8 × 102 cells to 8 × 105 cells per mouse) into naïve PKO hosts. The NP118-specific population of memory CD8+ T cells transferred exhibited a late memory phenotype (CD127hi, Apoptosis antagonist CD62Lhi, KLRG-1lo, CD27hi) and function (IL-2 and TNF cytokine production upon restimulation with NP118 peptide; Fig. 3A). All recipient

mice and a group that did not receive memory CD8+ T cells were challenged with LCMV-Arm. Mice receiving 8 × 105 and 8 × 104 NP118-specific memory CD8+ T cells rapidly lost weight and succumbed following LCMV infection (Fig. 3B and C). Interestingly, mice receiving 8 × 103 NP118-specific memory CD8+ T cells lost weight during the first week after LCMV infection but recovered without any mortality. On the other hand, mice receiving 8 × 102 NP118-specific memory CD8+ T cells exhibited only slight weight loss and did not succumb, similar to control mice that did not receive any memory CD8+ T cells (Fig. 3B and C). Consistent with their poor outcome, mice receiving either 8 × 105 or 8 × 104 NP118-specific

memory CD8+ T cells had high numbers (>107 cells/spleen) at 5 days post-LCMV infection (Fig. 3D). Importantly, a substantial fraction of NP118-specific secondary effector CD8+ T cells in the groups receiving the highest numbers Selleckchem MG 132 of memory CD8+ T many cells produced IFN-γ

directly ex vivo even in the absence of exogenous peptide stimulation (Fig. 3D). Together, these results suggested that secondary CD8+ T cells expansion and mortality in PKO mice are dictated by the starting number of NP118-specific memory CD8+ T cells at the time of LCMV challenge. Naïve PKO mice survive LCMV-Arm infection by exhausting their NP118-specific CD8+ T cells [[16]]. Furthermore, more than 98% of the CD8+ T cells response to LCMV infection in BALB/c mice is directed at the dominant NP118 epitope, with subdominant responses directed to GP283 and GP96 epitopes [[34, 35]]. Previous work showed that vaccination to generate wild-type memory CD8+ T cells against subdominant epitopes may be effective at protecting from both LCMV and LM infection [[36, 37]]. However, it remains unknown whether memory CD8+ T cells specific for subdominant LCMV epitopes will also lead to vaccine-induced mortality in perforin-deficient hosts. To address this issue, we immunized naïve PKO mice with 5 × 105 DC coated with either the dominant NP118 or subdominant GP283 LCMV epitopes, while mice in the control group received DC coated with a Plasmodium berghei CS252 epitope.