47 Acute dialysis was associated with increased hospitalization (17.9 vs 9.0 days) and mortality at 90 days (14% vs 6%). In a subsequent prospective study

of 178 patients, use of the algorithm led to increased dialysis access placement and reduction in acute dialysis from 50% to 23%. Holland and Lam studied a retrospective cohort of 201 predialysis patients.48 Independent predictors of in-hospital dialysis initiation were age (OR 1.038, 95% CI: 1.011–1.065), congestive heart failure (OR 2.877, 95% CI: 1.205–6.871) and shorter predialysis follow-up time (OR 0.945, 95% CI: 0.920–0.971). Every month lost due to late referral increased the risk of in-hospital commencement MK-8669 datasheet of dialysis by 5.5%. Jones et al. reviewed the GFR decline of 726 new patients with CKD stages 3–5 referred over a 6-year period.49 The rate of decline slowed from 5.4 mL/min per 1.73 m2 per year to 0.35 mL learn more after nephrological referral. This was associated

with a reduction in blood pressure and improved survival (HR 0.55, 95% CI: 0.40–0.75). Khan et al. analysed a retrospective cohort of 109 321 US Medicaid/Medicare patients who started dialysis between 1995 and 1998.50 Only 50% had received nephrological care in the 24 months preceding dialysis. Higher mortality was associated with age and visits to generalists and non-renal specialists. Compared with patients with three or more ‘months of nephrology care’ in the 6 months preceding commencement of dialysis, mortality was increased in those with no nephrological

care in the 24 months preceding dialysis (HR 1.51), no care in the 6 months preceding dialysis (HR 1.28) and Protirelin only 1–2 ‘months of nephrology care’ in the 6 months prior to dialysis initiation (HR 1.23). Ledoux et al. defined late referral as presentation to nephrology services less than 3 months prior to starting dialysis.51 In their cohort of 62 patients, biochemical indices were worse and initial duration of hospitalization increased in late referrals, however, 4-year mortality was not increased. Lenz et al., in a retrospective study of 170 patients starting dialysis, found that 92% started with temporary venous access.52 Absence of adequate predialysis care, failure to recover from acute renal failure and non-compliance with scheduled clinic appointments were the main reasons for this. He further suggested that the velocity of eGFR loss rather a given level of renal impairment may be a better trigger for access referral. Lhotta et al. divided a cohort of 75 patients into 33 early referral and 42 late referral (defined as GFR <20 mL/min per 1.73 m2.53 Late referred patients had higher comorbidity. By univariate analysis, comorbidity and age were significantly associated with mortality, whereas in multivariate analysis, only comorbidity was associated with higher 2-year mortality.

As previously described 54, immunoprecipitations were performed with an anti-CD16 mAb (clone 3G8, mice IgG1, BD biosciences) or an anti-EGFR mAb (mice IgG1, Santa Cruz, Heidelberg, Germany) and sera of

non-immunized mice (Dako) used as the negative control. Immunoblotting was performed using Nupage Adriamycin price system (Invitrogen) and L1 proteins from VLPs were detected using CAMVIR antibody (Abcam, Cambridge, UK) and Clean Blot IP detection reagent (Thermo Fisher). The assay to detect activated GTPase proteins was carried out as previously described 55. Briefly, cells were lysed by addition of 200 μL of ice-cold lysing buffer. Lysates were centrifuged for 5 min at 16 000×g. Supernatants were immediately frozen in liquid nitrogen and stored at −80°C until use. For pull-down assays, supernatants were incubated for 30 min with 30 μg of GST-PBD protein containing the Cdc42 and Rac1 binding regions of PAK-1B, affinity linked to glutathione-sepharose beads. The beads were washed in ice-cold washing buffer and boiled in SDS-PAGE lysis buffer. The amount of Rac1 and Cdc42 in the samples was Ivacaftor nmr determined by immunoblotting with antibodies specific to Rac1 (23A8, Upstate Biotechnology,

Waltham, USA) and Cdc42 (BD Biosciences). Prism 4.0 (GraphPad Software) was used for data handling, analysis and graphic representation. Statistical analysis was performed using Student’s t-test or the Mann–Whitney test. The authors thank Dr. S. Ormenese from the GIGA-Imaging and Flow Cytometry platform for her support with flow cytometry and confocal microscopy and Prof. N. Antoine for the preparation of electron microscopy grids. They are also grateful to Dr. P. Coursaget for the provision of baculovirus expressing HPV16 and HPV31 L1, Dr. L. Bousarghin for providing electron microscopy grids with DCs containing HPV-VLPs, Prof. N. Christensen for providing

V5 antibodies, Carteolol HCl M. Lebrun for her assistance with confocal microscopy, Dr D. Begon for her advice on co-immunoprecipitation and Prof. G. Thibault for helpful discussion. They thank GlaxoSmithKline Biologicals for providing polyclonal antibodies used to assess the quality of L1-VLPs by ELISA. This study was supported by the Belgian National Fund for Scientific Research (FNRS), C. D., A. C. and N. J. are supported by the FNRS. V. R., B. B. and I. L. are supported by a Télévie grant from the FNRS. Conflict of interest: The authors declare no financial or commercial conflict of interest. Detailed facts of importance to specialist readers are published as ”Supporting Information”. Such documents are peer-reviewed, but not copy-edited or typeset. They are made available as submitted by the authors.

We are most grateful to the patients and controls who generously donated blood samples and to Dr Misbah, Dr Lorton and Dr Patel, who care for these patients. We are also grateful to the staff at the Department of Clinical Laboratory Immunology at the Churchill Hospital, Oxford for their support and performing the lymphocyte subset analyses. Authors’ conflicts of interest: None declared. “
“Natural killer (NK) cell adoptive

transfer is a promising approach for cancer immunotherapy; however, its AZD3965 cost development has been hindered by the lack of efficient methods to produce large numbers of functional NK cells. In this study, we engineered the leukaemia cell line K562 to express this website CD137 ligand (CD137L) and membrane-bound interleukin (mbIL)-21 on the cell surface, and used these cells to expand NK cells from the peripheral blood mononuclear cells. We found that purity of the NK cells (CD3−CD56+/CD16+) increased from less than 30% to above 95% after a 3-week expansion and proliferation of the cells was sustained for more than 8 weeks. The surface expression

of NK cell activating and inhibitory receptors, except for NKp80, was clearly increased with the expansion, and NK cell-mediated killing activity was also enhanced significantly. However, these changes in both phenotype and function were clearly reversed by JSI-124, a specific signal Silibinin transducer and activator of transcription-3 (STAT-3) inhibitor. Taken together, data showed that the combination of mbIL-21 and CD137L could efficiently induce the formation of functional human NK cells from peripheral blood mononuclear cells, and STAT-3 inhibition could impair this induction. Therefore, STAT-3 activation may benefit human NK cell proliferation and cytotoxicity, and provide valuable clinical applications in NK cell immunotherapy against viral infectious diseases and cancers.

Human natural killer (NK) cells are a subset of peripheral blood lymphocytes that are defined by their expression of CD56 and/or CD16 and the absence of T cell receptor CD3 [1]. NK cells can recognize and subsequently kill virus-infected and transformed cells in the absence of prior stimulation, and play a critical role in the immune surveillance of virus infectious diseases and cancers. NK cell killing is regulated through balanced signals from the activating and inhibitory receptors on NK cell surface [2]. A large number of studies have demonstrated that NK cells could elicit strong anti-tumour efficacy, and are promising effectors for adoptive immunotherapy against cancers [3]. NK cell alloreactivity could control leukaemia relapse without causing graft-versus-host disease (GVHD) [4]. Adoptive transfer of NK cells has been tested in early-phase clinical trials and has emerged as a safe and potentially efficacious immunotherapy for cancers [5].

14 The length of this insertion inversely correlated with the age at onset in patients. Dissecting selleck chemicals llc molecular mechanisms of 16q-ADCA, newly renamed

as SCA31, would be an important theme to discover the pathologic basis of this peculiar morphological change. We would like to thank Dr Taro Ishiguro (Tokyo Medical and Dental University) for assisting graphics in this article. This paper is based on a long history of study discovering the clinical, genetic and neuropathological characteristics of 16q-ADCA, now renamed as SCA31. We would like to acknowledge all the people who participated in this study. Particularly, we are in debt to Dr Kiyoshi Owada (Tokyo Medical and Dental University), Drs Gen Ishida and Manabu Gomyoda (Matsue National Hospital), Drs Mari Yoshida and Yoshio Hashizume (Aichi Medical College), Dr Toshio Mizutani (Tokyo Metropolitan Neurological Hospital), Dr Kunihiro Yoshida

(Shinshu University), and Drs Yuko Saito and Shigeo Murayama (Tokyo Metropolitan Geriatric Institute) for sharing their neuropathological samples. We also acknowledge Dr Asao Hirano (Montefiore Medical Center) for providing us specimens with Menkes’ disease as a control. “
“We examined a solitary hematoma in a patient with sporadic cerebral amyloid angiopathy (CAA). The hematoma affected the middle frontal sulcus, cerebral CHIR-99021 cortex (CC) and subcortical frontal white matter (sfWM). We embedded the hematoma in four paraffin blocks, each of which was cut serially into 6-µm-thick sections. The first section and every 18th section from each block

were subjected to Elastica-Goldner (E-G) staining, and the distribution and diameter of the ruptured blood vessels (rBVs) were examined. The rBVs were then marked on diagrams representing each E-G-stained section. The present study yielded the following important findings: (i), early- and recently ruptured Aβ-positive arteries were present mainly in the intrasulcal hematoma (ISH), rather than in the CC; (ii) many early-ruptured arteries this website in the ISH were larger in diameter than those in the CC; and (iii) ruptures of the cortical arteries, even near the cortical surface, did not occur so frequently and the ruptured vessels were small in size. We concluded that in patients with subcortical hematoma caused by sporadic-type CAA, successive rupturse of the meningeal vessels, mainly arteries, occur in the cerebral sulcus initially, followed by formation of an ISH and development of a fresh hemorrhagic or anemic infarct in the CC surrounding the ISH, the latter in most cases then extending into the brain parenchyma through the necrotic CC at the depth of the sulcus, finally creating a secondary hematoma in the subcortical white matter. “
“Fatty acid synthase (FASN) and carnitine palmitoyltransferase 1C (CPT1C), a brain-specific isoform of the CPT1 family, are upregulated in certain types of cancers, including gliomas.

We injected the adenoviruses encoding TDP-43, FUS and shRNAs for protein degradation pathways into the facial nerve and let the viruses transfer to the facial motoneurons via retrograde axonal transport, and express the virus-induced foreign genes in the motoneurons. Approximately 10–30% of facial motoneurons were successfully labeled with DsRed and/or EGFP after the adenovirus injection. Similar to in vitro experiments as described above, adenovirus-induced wild type and CTF TDP-43 were localized exclusively in the nucleus and in

the cytoplasm in a diffuse manner, respectively selleckchem (Fig. 5A,B). Mutated TDP-43 proteins induced by adenovirus infection were also localized predominantly in the nucleus and rarely in the cytoplasm (Fig. 5C). We did not observe aggregate formation in either of these infected motoneurons. We then injected mixed suspensions of adenoviruses expressing TDP-43 and shRNAs into the facial nerve. Injection of mixtures of adenoviruses expressing wild type and CTF TDP-43, and shRNAs for protein degradation pathways PSMC1, ATG5 or VPS24 induced cytoplasmic aggregate formation in facial motoneurons (Fig. 5D–F). Similar aggregates were also formed when mutated TDP-43 was used instead

of wild type TDP-43 for combined injections (Table 2). To examine these aggregates under the electron microscope, Panobinostat order serial glutaraldehyde/paraformaldehyde-fixed vibratome sections of 50 μm thickness were made from brain stem tissues containing facial nuclei. We took photographs of the aggregate-bearing motoneurons in these sections under the fluorescent microscope, and the sections were embedded in Epon 812. Semithin sections were serially made and we identified the individual aggregate-bearing motoneurons in toluidine

blue-stained sections. We then made ultrathin sections and examined them under the electron microscope. As shown in Figure 6, cytoplasmic aggregates were identified in facial motoneurons co-infected with wild type and CTF TDP-43 and PSMC1 shRNA adenoviruses 7 days postoperation. These cytoplasmic aggregates were non-membrane bound and composed of electron-dense PAK5 granular materials and some filamentous structures (Fig. 6D,E). Similar cytoplasmic aggregates were also seen in facial motoneurons co-infected with wild type and CTF TDP-43 and ATG5 shRNA adenoviruses 7 days postoperation (Fig. 7). In these non-membrane-bound aggregates, some filamentous structures of 15–25 nm in diameter were seen among the granular materials (Fig. 7D–G). Concentric lamellar structures containing mitochondria and vesicles were also seen close to the aggregates, suggesting an impairment of autophagic flux due to ATG5 shRNA adenovirus infection (Fig. 7E).

18 Chromatin immunoprecipitation experiments have shown binding of NFAT1 to promoter of IL-4 in Th2 cells but not in Th1 cells, suggesting chromatin remodelling as one of the mechanism that determines NFAT binding to its target genes.19 NFAT is also the major player in the ionomycin-induced anergy click here model.20 Anergy is defined as a state of

T cells where they are unresponsive to stimulation and fail to make IL-2 or proliferate.21 An anergic state is achieved when T cells are stimulated through the TCR in the absence of co-stimulation in vitro.22 Developed by Rao and colleagues, the ionomycin-induced anergic state is achieved by treating cells with the calcium ionophore for a period of about 12 hr subsequent

to which cells become unresponsive to TCR stimulation and fail to make IL-2 or proliferate. This form of anergy is largely NFAT dependent because sustained high calcium levels cause cells to primarily activate RG7204 research buy NFAT. A constitutively active form of NFAT when expressed in T cells also leads to a similar state.20 The NFAT rapidly translocates to the nucleus on a rise in intracellular calcium. Several studies indicate that NFAT translocation into the nucleus is more efficient if the calcium signal is oscillatory.23,24 Within minutes of reducing the cytoplasmic calcium level, NFAT is rapidly exported out of the nucleus. In another cell type these kinetics were much slower.25 Hence, the re-phosphorylation kinetics may differ from cell type to cell type. Because the formation of the immune synapse is preceded by calcium fluxes,5,26 the transport of NFAT into the nucleus in T cells is presumably rapid. Recently a novel regulation for NFAT-like proteins was described. Crz1 is a calcineurin-dependent transcription factor in yeast

wherein it plays an important role in stress-induced apoptosis. Elowitz and colleagues monitored the real-time trafficking Ribociclib purchase of Crz1 fused to green fluorescent protein in response to increasing extra-cellular calcium. They found that the amount of Crz1 translocated to the nucleus was not simply proportional to the concentration of extra-cellular calcium. Instead, Crz1 translocated into and out of the nucleus in oscillatory bursts. Neither the amplitude nor the duration of these bursts changed as extra-cellular calcium was increased; rather, the frequency of bursts increased. The authors further showed by mathematical modelling and experimental validation that the frequency-modulated trafficking of Crz1 was important for maintaining the same amount of relative gene expression across different Crz1 targets as the extra-cellular stimulus changed.27 As NFAT is calcineurin dependent, it would be interesting to see if this form of regulation is valid for NFAT in mammalian cells.

5–2 h (cold ischaemia time) before being implanted into the recipient. The recipients were also anaesthetized with ekviticine and placed on a heated operating table. The left kidney was removed, and the pancreatic-duodenal selleck graft was anastomosed to the renal

blood vessels by a non-suturing cuff technique as previously described [17]. The graft duodenum was sutured end-to-side to a loop of the colon of the recipient with 7–0 silk. After closure of the abdominal wound, the animals were injected subcutaneously with 10 mg doxycycline (Idocyclin™; AB Leo, Malmö, Sweden) and were observed until fully recovered from anaesthesia. The animals were surgically prepared for blood flow measurements as given above, 2 days after transplantation. The blood flow values to the endogenous and transplanted pancreases, the islets in both glands and the endogenous and transplanted duodenum were measured with the microsphere technique referred to above. Histological examinations.  After blood flow measurements samples from

both the endogenous and transplanted pancreases were fixed in 4% buffered (pH 7.3) formalin with 1% cetylpyridinium chloride (Sigma). These samples were then dehydrated, embedded in paraffin, sectioned (4 μm thick) and stained with haematoxylin and eosin. The slides CB-839 were then examined by an observer unaware of the origin of the samples especially for the presence of interstitial oedema, infiltrating cells and vacuoles within acinar or endocrine cells. In the non-transplanted animals, the endogenous pancreas was removed and studied similarly. Assay of HA and determination of water content.  Samples from oxyclozanide both the endogenous and transplanted pancreases and duodenum (approximately 25–35 mg each) were taken from the caudal portions of the glands, or the peri-ampullar region of the intestines. In non-transplanted animals, samples were only taken from the caudal part of the endogenous pancreas. The specimens were put on filter paper and weighed 3 min later to obtain the wet weight. The samples were then lyophilized and weighed again to obtain the dry weight. The

specimens were ground, and HA were extracted for 16 h with 0.5 m sodium chloride. Supernatants, obtained after centrifugation at 2000 g for 15 min, were analysed for HA content with a radiometric assay (Pharmacia & Upjohn Diagnostics, Uppsala, Sweden) as previously described in detail [18]. Standard curves were constructed from samples with known amounts of HA, and double analyses were performed on all samples. The variability was <10%. The relative water content, expressed as per cent water of the total weight of the tissue, was calculated as 100 × (wet weight – dry weight)/wet weight. An initial study was performed in which the measurements were made in transplanted animals on day 2, 4 or 7 post-transplantation. Based on these findings, blood flow measurements and analyses of HA and water contents were performed day 2 post-transplantation.

Several authors [2, 37, 38] described protective effect

of antibodies against experimental disseminated candidiasis in vivo. Prepared monoclonal antibodies showed enhanced ingestion and killing of yeast cells by PMN (MAb B6.1) or macrophages (MAb C7) in the presence of serum complement [37, 38]. They proposed that complement activation might contribute to the protection by antibodies in vivo and that during initiation of candidiasis protective antibodies induce prompt complement opsonization, which results into an association of Candida cells with host phagocytes. Non-protective antibodies may lead to reduced complement activation kinetics. According these results, we could assume enhanced candidacidal RG-7388 in vitro activity induced by serum opsonization in vitro as a possible precondition for protection in vivo. Differences concerning the antibody quantity, specificity and isotype composition of polyclonal sera could explain why antibody protection against Candida infection has been observed in some studies but not in the others. Presented study indicates limited effectiveness of branched α-mannooligosides to induce production of highly protective antibodies. Additional and more detailed immunomodulatory properties

investigation of α-mannooligosides of different structure should bring significant information to successful protective anti-Candida subcellular vaccine development. This project was supported by grants from Grant Agency of Slovak Academy of Sciences VEGA No.

2/0026/13, by the Slovak Research GSK1120212 and Development Agency under the contract No. APVV- 0032-06. This contribution is the result of the project implementation: Centre of excellence for Glycomics, ITMS 26240120031, supported by the Research & Development Operational Programme funded by the ERDF. “
“Biological Research Department, Drug Discovery and Biomedical Technology Unit, Daiichi Sankyo RD Novare Co., Ltd., Tokyo, Japan Germinal centers (GCs) are generally considered to be the sole site of memory B-cell generation. However, recent studies demonstrate that Carnitine palmitoyltransferase II memory B cells can also develop in response to a T-cell dependent (TD) antigen before the onset, and independently of, the GC reaction. These two classes of memory cells persist equally over long periods of time and attain functional maturation through distinct but related transcriptional programs. Although the development of both memory B-cell types requires classical T-cell help, the generation of GC-dependent memory B cells requires TFH-cell help, while the generation of GC-independent memory cells does not. These findings led to the conclusion that B-cell memory is generated along two fundamentally distinct cellular differentiation pathways. In this review, we focus on the GC-independent pathway of memory B-cell development, and discuss how the unique features of memory B cells are maintained in the GC-independent pathway.

Nucleus was counterstained with Hoechst 33342. Images were captured with wide-field fluorescence Leica DMIRE2 microscope coupled to a monochromator (Polychrome IV from Till Photonics, Lochhamer Schlag, Germany) and CCD camera (CoolSNAP HQ; Photometrics, Tucson,

AZ, USA). Data were analysed with GraphPad Prism (GraphPad Software Inc, San Diego, CA, USA). The Kruskall–Wallis test, Mann–Whitney U-test or Wilcoxon’s matched-pairs test were used when appropriate. Differences were considered significant at P < 0·05. Sputum samples were obtained from 24 asthma patients and 18 control subjects. The mean FEV1 of the 24 asthma patients was 2623 ml (94·5%) and the mean FVC was 3320 ml (100·4%), Venetoclax while the FEV1/FVC ratio was 76·73. The distribution of asthma according to severity and current therapy using GINA guidelines was as follows: mild intermittent (n = 0), mild persistent (n = 1), moderate persistent (n = 15) and severe persistent (n = 8). Atopy was found in 12 of 24 asthma patients. Two of 24 asthma patients and eight of 18 control subjects had a

history of smoking. All healthy controls had normal spirometry and all participants denied clinical symptoms of upper or lower airway disease during the previous 4 weeks and the use of anti-asthma medication in the last 5 years. Clinical characteristics of patients are shown in Table 1. The quality of induced sputum samples was determined by the presence AUY-922 of < 20% squamous epithelial cells and > 50% cell viability assessed by vital dye 7-AAD exclusion. The samples that did not fulfil quality criteria were excluded from the study. Differential cell count obtained from cytospin preparations are shown in Table 2. FACS analysis of single-cell suspensions stained for cell surface markers detected a predominance of leucocytes (CD45+, 60–90%), most of which were CD16+. Representative flow histograms are shown in Supplementary Fig. S1. The expression of gal-1, gal-3 and gal-9 were

analysed by RT–PCR in cells isolated of induced sputum samples from asthma Sucrase patients and healthy control subjects. Gal-1 and gal-3 mRNA levels in samples from asthma patients [mean ± standard error of the mean (s.e.m.) = 2·6 ± 0·4 and 4·4 ± 1·4, respectively] were lower than those from healthy subjects (4·7 ± 1·2 and 20·0 ± 8·7) (Fig. 1a). In contrast, gal-9 mRNA expression did not vary significantly between the two groups (3·2 ± 1·3 versus 3·3 ± 1·1) (Fig. 1a). As expected, sputum samples from asthma patients contained elevated mRNA levels of the Th2 cytokines IL-5 and IL-13 (P < 0·05, Fig. 1b). The Th17 response has been proposed recently to play an important role during the pathology of allergic asthma [21]. However, the Th17 cytokines IL-17 and IL-23 were undetectable in sputum samples under our experimental conditions (data not shown). Surface expression of galectin proteins in sputum cells was determined by flow cytometry.

The harvested BMDC were divided into groups and further cultured for 18 hr in medium alone as control or in the presence of rHp-CPI, LPS, CpG, LPS plus rHp-CPI or CpG plus rHp-CPI. The BMDC were stained and analysed for the expression of co-stimulatory and

MHC-II molecules. The results show that treatment of the immature DC with rHp-CPI alone reduced the expression of the MHC-II molecule but did not alter the frequencies of CD11c+ DC that express CD40, CD80 and CD86 and the expression levels of these molecules compared with medium control group (Fig. 5a,b). The immature DC stimulated with LPS showed significantly increased expression of CD40 and CD80 (both the frequencies of positive cells Protein Tyrosine Kinase inhibitor and the MFI) compared with medium control, and rHp-CPI treatment reduced the increased CD80 expression in response to LPS stimulation, but had no effect on CD40 expression (Fig. 5a,b). CpG stimulation of the immature BMDC also induced enhanced expression of CD40 and CD80. The rHp-CPI inhibited the increased expression of CD40 and CD80 induced by CpG (Fig. 5a,b). We further examined the cytokine production by BMDC and observed that the differentiated immature

BMDC with or without rHp-CPI treatment produced minimal levels of IL-6, IL-12p40 and TNF-α. Stimulation of the immature BMDC with LPS and CpG induced increased production PKC412 of these pro-inflammatory cytokines. The rHp-CPI treatment reduced the IL-6 production induced by both LPS and CpG, and TNF-α production induced by CpG (Fig. 5c). These results show that although treatment of rHp-CPI alone did not alter immature BMDC co-stimulatory molecule expression and cytokine production, it modulates these activation responses of DC induced by LPS and CpG. To determine whether the T-cell activation function of DC is altered by rHp-CPI, DC and CD4+

a T-cell co-culture assay was performed. Bone marrow cells were cultured in the aminophylline medium containing GM-CSF as described above. The immature BMDC were harvested on day 7, re-plated and cultured for 24 hr to obtain matured DC. Mature BMDC were incubated either in medium alone or with rHp-CPI for 2 hr and then pulsed with OVA antigen. The two groups of DC were then co-cultured with OVA-specific CD4+ T at the ratio of 1 : 2. As shown in Fig. 6(a), BMDC treated with rHp-CPI before OVA antigen pulsing induced a lower level CD4+ T-cell proliferation response than the BMDC that were pulsed with OVA only. CD4+ T cells co-cultured with BMDC that were treated with rHp-CPI and pulsed with OVA produced significantly less interferon-γ than the CD4+ T cells co-cultured with BMDC pulsed with OVA only (Fig. 6b). In this DC and CD4 T-cell co-culture, no significant levels of IL-4, IL-10 and IL-13 were detected. Adoptive transfer of BMDC was performed to further assess the effect of rHp-CPI on the function of DC. Mice were transferred with enriched BMDC that were pulsed with OVA with or without pre-treatment of rHp-CPI and boosted 4 weeks later with OVA antigen.