There was variable overlap between CD34 and nestin positivity within the micronodular and/or MG-132 clinical trial ganglioglioma-like areas. Conclusions:

Immunoreactivity for CD34 and nestin characterizes the dDNT and helps to distinguish it from other lesions associated with epilepsy. Histological evidence indicative of transition of dDNT to other forms of DNT and ganglioglioma suggests that dDNT might be an early histogenetic form of these glioneuronal tumours. “
“Disability after traumatic spinal cord injury (TSCI) results from physical trauma and from “secondary mechanisms of injury” such as low metabolic energy levels, oxidative damage and lipid peroxidation. In order to prove if early metabolic reactivation is a better therapeutic option than antioxidant therapy in the acute phase of TSCI, spinal cord contusions were performed in adult rats using a well-characterized weight

drop technique at thoracic 9 level. After TSCI, pyrophosphate of thiamine or non-degradable cocarboxylase (NDC) enzyme was used to maintain energy levels, antioxidants such as superoxide dismutase and catalase (ANT) were used to decrease oxidative damage and methylprednisolone (MP), which has both therapeutic properties, was used as a control. Rats were divided into one sham group and six with TSCI; one of them received no

treatment, and the rest Selumetinib see more were treated with NDC, MP, NDC + MP, NDC + ANT or ANT. The ANT group decreased lactate and creatine phosphokinase levels and increased the amount of preserved tissue (morphometric analysis) as well as functional recovery (Basso, Beattie and Bresnahan or BBB motor scale). In contrast, NDC treatment increased lipid peroxidation, measured through thiobarbituric acid reactive substances (TBARS) levels, as well as spinal cord tissue destruction and functional deficit. Early metabolic reactivation after a TSCI may be deleterious, while natural early metabolic inhibition may not be a “secondary mechanism of injury” but a “secondary neuroprotective response”. While increased antioxidant defence after a TSCI may currently be an ideal therapeutic strategy, the usefulness of metabolic reactivation should be tested in the sub-acute or chronic phases of TSCI and new strategies must continue to be tested for the early ones. “
“K. T. Wong, K. Y. Ng, K. C. Ong, W. F. Ng, S. K. Shankar, A. Mahadevan, B. Radotra, I. J. Su, G. Lau, A. E. Ling, K. P. Chan, P. Macorelles, S. Vallet, M. J. Cardosa, A. Desai, V. Ravi, N. Nagata, H. Shimizu and T.

Here, we rederived ChAdV-68 [37] (also called SAdV-25, C68, and Pan9), inserted its whole genome into bacterial artificial chromosome (BAC), deleted the E1 and E3 regions, and inserted

a consensus clade B https://www.selleckchem.com/products/17-AAG(Geldanamycin).html Gag Tg expression cassette into its genome at the E1 locus. The resulting ChAdV68.GagB vaccine was evaluated for protective efficacy in combinations with plasmid pTH.GagB DNA and modified vaccinia virus Ankara MVA.GagB. This work extends on previously published mouse data [17, 20], and parallels rhesus macaque [11, 19, 21] and ongoing phase I/IIa clinical trial [38] studies exploring similar regimens. Although SAdV-25 had previously been cloned as an E1-deleted vector AdC68 [37, 39], we generated an independently Selleckchem Dabrafenib derived E1

and E3 region deleted vector, here referred to as ChAdV-68, from WT SAdV-25 genomic DNA. Rather than traditional and laborious ligation-based methods, we used two new restriction site-independent approaches to precise deletion of E1 and E3 regions from the adenovirus genome as described elsewhere [40]. Briefly, the first method of Chartier et al. [41] was modified to enable E1 deletion concomitant with recombination of the viral genome into the destination plasmid (see Materials and Methods). Of four clones analyzed, all contained the viral genome and three contained the intended E1 deletion, resulting from recombination downstream rather than upstream of the E1 locus. Having used a BAC rather than a multicopy plasmid backbone, we were then able to employ GalK recombineering [42] to delete the E3 region and replace it with a unique PmeI site, an approach that exhibited 100% efficiency. Complete shotgun sequencing of the resulting E1 and E3 deleted ChAdV-68-BAC clone revealed that it was identical to the SAdV-25 reference sequence (NCBI RefSeq accession no. AC 000011) with the exception of five single-nucleotide differences at positions 8919 (C to

G, Gly to Arg in preterminal protein), 15758 (G to C, silent), 17156 (A to ADAM7 T, intergenic), 17434 (C to A, intergenic), and 35228 (G to C, His to Gln in E4). In order to directly confirm and extend published data on chimpanzee adenovirus serotype 68 vectored vaccines expressing HIV-1 clade B Gag [17-20], ChAdV68.GagB was constructed. A synthetic gene using humanized codons coding for myristoylated full-size consensus HIV-1 clade B p55Gag polypeptide (Genbank accession no. AAS19377) was coupled to an mAb epitope Pk at its C-terminus to facilitate detection and the chimeric gene GagB was inserted into the adenovirus genome at the E1 locus under control of the CMV major immediate-early promoter. To assess the ChAdV68.GagB vaccine in heterologous prime-boost regimens, vaccines expressing GagB vectored by plasmid DNA pTH.GagB and modified vaccinia virus Ankara MVA.GagB were also constructed. Expression of the GagB protein in human cells was confirmed by immunofluorescence (Fig. 1A) and on a western blot of infected/transfected cell lysates (Fig.

In agreement with this prediction, in this study we have shown that autoreactive CD8+ T cells bearing the aggressive 8.3 transgenic TCR also require IL-21 to initiate

T1D. We have also shown that CD8+ T cells from 8.3-NOD.Il21−/− mice proliferate poorly to antigen stimulation and that this defect results, at least partly, from reduced Il2 gene expression. Two recent studies have addressed the pathogenic mechanisms of IL-21 in T1D. Using the spontaneous NOD CX-4945 manufacturer T1D model, McGuire et al. have shown that IL-21 secreted by a subset of CD4+ helper cells that express CCR9 and infiltrate the islets is needed for CD8+ T cell expansion and survival [9]. Van Belle and colleagues used a virus-induced T1D model that implicated IL-21 in facilitating DCs to transport antigens from pancreas to draining lymph nodes in order to activate CD4+ T cells, which then provide help to CD8+ T cells [11]. In the 8.3-NOD mouse model used in our study, the transgenic TCR allowed us to evaluate directly the antigen responsiveness of CD8+ T cells, revealing a fundamental defect in the ability of Il21−/− 8.3 T cells to undergo efficient antigen-induced proliferation. A similar defect in the expansion of viral antigen-specific CD8+ T cells has been shown to occur in Il21−/− and Il21ra−/− mice, which fail to clear chronic viral infection [27-29, 45]. Even though these studies have shown

that IL-21 acts directly on viral antigen-specific CD8+ T cells Rucaparib to sustain their expansion in a cell autonomous manner, the Protease Inhibitor Library ic50 underlying mechanisms remain unclear. In Il21−/− mice, antigen-specific

CD8+ T cells showed an elevated expression of the inhibitory receptor programmed death 1 (PD-1) 5 months after infection [27, 28]. However, IL-21 deficiency did not affect PD-1 expression during primary or secondary responses following acute viral infection [31]. In another study, defective antigen-specific CD8+ T cell expansion in Il21ra−/− mice was correlated with elevated expression of TRAIL, a TNF-related apoptosis-inducing molecule implicated in activation-induced cell death [30]. In 8.3-NOD mice, CD8+ T cells bearing the transgenic TCR would constantly encounter the endogenous autoantigen, akin to chronic stimulation. However, we did not observe up-regulation of either PD-1 or TRAIL in freshly isolated 8.3 T cells from 8.3-NOD.Il21−/− mice, nor were these molecules modulated differentially upon antigen stimulation (data not shown). Studies examining the role of IL-21 in anti-viral responses concur that IL-21 exerts a cell autonomous effect on CD8+ T cells to sustain their proliferative potential [45]. These studies have shown normal or even elevated IFN-γ production by viral antigen-specific CD8+ and CD4+ T cells from Il21−/− and Il21ra−/−-deficient mice, and normal IL-2 production by CD4+ T cells from virus-infected Il21ra−/− mice [28, 29, 31].

This newly developed animal model now includes three major hallmarks Depsipeptide of AD: genetically related age-dependent β-amyloidosis and tau hyperphosphorylation, complemented with experimentally induced cholinergic cell loss. Prospectively, such an attempt using 3xTg mice with modifiable cholinergic dysfunction appears promising for studies addressing different aspects of this devastating disease. Currently, acetylcholinesterase

inhibitors are still, despite their limitations, the most widely used drugs for symptomatic AD therapy [81]. Selective α7 nicotinic acetylcholine receptor partial agonists are now in clinical trials and have been demonstrated to be beneficial in preclinical studies by potentiating the acetylcholine response of α7 nicotinic acetylcholine receptors [82]. The presented data support the view that drugs targeting the cholinergic neurotransmission remain justified as a potential treatment strategy of AD (for review see [47]). The authors thank Drs Reinhard Schliebs and Thomas Arendt for critical reading of an earlier version from this article. We are

thankful to Dr Peter Davies (Pathology, Albert LEE011 mw Einstein College of Medicine, New York, USA), Dr Sascha Weggen (Neuropathology, University of Düsseldorf, Germany) and Dr Christian Czech (Hoffmann-La-Roche, Basel, Switzerland) for the donation of antibodies and Drs Frank M. LaFerla and Salvatore Oddo (University of California, Irvine, CA, USA) for pairs of triple-transgenic and WT mice. The technical assistance of Dr Anke Hoffmann, Ute Bauer and Marita Heindl is gratefully acknowledged. The biochemical part of the study was supported by the Alzheimer Forschung Initiative e.V. (to O.W.). The study was designed by Wolfgang Härtig who also performed the histological work together with Simone Goldhammer (SG) as part of her MD thesis. Immunolesions were made by Johannes Kacza. All biochemical data were generated by Annika Saul and Oliver Wirths. Histological CHIR-99021 cost figures were produced by Jens Grosche, Simone Goldhammer and Dominik Michalski. The manuscript was written

by Wolfgang Härtig and considerably improved by Oliver Wirths and Dominik Michalski. “
“Upon denervation, skeletal muscle fibres initiate complex changes in gene expression. Many of these genes are involved in muscle fibre remodelling and atrophy. Amyotrophic Lateral Sclerosis (ALS) leads to progressive neurodegeneration and neurogenic muscular atrophy. Disturbed calcium homeostasis and misfolded protein aggregation both in motor neurons and muscle fibres are key elements of ALS pathogenesis that are mutually interdependent. Therefore, we hypothesized that the calcium sensor STIM 1 might be abnormally modified and involved in muscle fibre degeneration in ALS and other types of NMA. We examined ALS and NMA patient biopsy and autopsy tissue and tissue from G93A SOD1 mice by immunohistochemistry and immunoblotting.

For the original untreated negative control iDCs, after

cell transfer to a new 24-well plate, one well still remained untreated whereas Panobinostat order the other well was treated with LPS. After another 24 hr (Day 2), contents of each well were collected for either cell or cytokine assays. After DC treatment with chemokines (Day 1) and subsequent LPS stimulus (Day 2), cell viability was also determined using Trypan blue exclusion. All treatments and controls exhibited at least 90% viable cells (data not shown). Hereafter, any combination of CCL3 and CCL19 at a specific ratio will adhere to the nomenclature: CCL3 + 19 (ratio). To measure the endocytic capacity of DCs upon chemokine or subsequent LPS treatment, DCs were incubated with fluorescently labelled OVA 24 hr after chemokine treatment (Day 1) or 24 hr after subsequent LPS treatment (Day 2) and the amount of OVA

internalized by DCs was determined using flow cytometry. Immature DCs treated with individual chemokines or chemokine combinations exhibited endocytic capacity comparable to untreated iDCs (Fig. 2a). As expected, upon subsequent LPS maturation, iDCs treated only with LPS reduced their PLX4032 in vivo endocytic capacity significantly compared with untreated iDCs. However, iDCs pre-treated for 24 hr (Day 1) with individual chemokines or an equal Thalidomide combination of CCL3 + 19 (5 : 5), then subsequently treated with LPS exhibited an endocytic capacity similar to untreated iDCs. Surprisingly, even after subsequent

LPS treatment, iDCs pre-treated with CCL3 + 19 (7 : 3) showed an endocytic capacity 36% higher than untreated iDCs, whereas iDCs pre-treated with CCL3 + 19 (3 : 7) exhibited a 30% lower endocytic capacity than untreated iDCs (Fig. 2a,b). When endocytic capacity (MFIs by flow cytometry) was recalculated, now normalized to the value of endocytic capacity for untreated iDCs on Day 1, iDCs pre-treated with CCL3 + 19 (7 : 3) retained 57% of their endocytic capacity, even after subsequent LPS treatment. Conversely, the normalized endocytic capacity of untreated iDCs or iDCs treated with only LPS was reduced to 44% or 15%, respectively (Fig. 2c). Even though there is no direct evidence explaining why the endocytic capacity of untreated iDCs decreased over time, this natural decrease was presumably attributed to effects of the GM-CSF in the culture media[41-43] and of the cell transfer (Fig. 1)[41] on minimal maturation of these DCs during the 3-day culture in this study.

, 1998). Here, we tested how different routes of immunization can be used to generate immune responses inducing a protection against CDI, with Cwp84 as an antigen. Immunizations by the intragastric route did not induce an increase of seric Cwp84-specific antibody levels and this result was correlated with the very low animal protection from CDI observed. Antigen degradation by gastric

and intestinal secretions, dilution in the intestinal fluids, poor sampling via Peyer’s patches, may all be factors that contribute to the limited efficiency of the oral route. It seems evident that this route requires that antigens selleck must be protected from degradation by digestive enzymes. The subcutaneous route was the best to induce a high systemic immune response with antibody titres more than twofold higher than that for the intrarectal route. However, in this study, serum Cwp84 antibody titres did not correlate with protection. The best animal protection was observed with the rectal route of immunization. Further studies are needed to specify the immune effectors induced by rectal immunization. Unfortunately, secondary antibodies directed to hamster IgA are not commercially available. This is why we were not able to determine more precisely the specific immune response at the intestinal level. We failed to find evidence of significant neutralization activity against the Cwp84 protease activity in the serum of hamster vaccinated with a protective intrarectal formula

vaccine. These results indicate Miconazole FK228 solubility dmso that, in this model, protection is probably not only related to neutralizing antibodies and other factors may play an important role in the host immune response against CDI. Because survival correlated poorly with antibodies titres, it is possible that our immunization strategy generated a wider cell-based immunity that induces partial protection. Recent

data on Streptococcus pneumoniae have demonstrated that multiple immune cell types are required for the induction of a protective immunity in a murine model that lacks mature B cells and fails to produce antibody (Mizrachi-Nebenzahl et al., 2003; McCool & Weiser, 2004). Recently, surface proteins such as the SLPs, because they cover the cell almost completely, have been tested in a series of immunizations combined with different systemic and mucosal adjuvants and challenge experiments in Golden Syrian hamsters (Ni Eidhin et al., 2008). None of the immunization regimens conferred complete protection in the hamster model, and antibody stimulation was variable within regimens, and generally modest. Others have demonstrated the benefits of using a protease as components of vaccines against S. pneumoniae for example. Mucosal immunization with caseinolytic protease (ClpP) antigen induced both systemic and mucosal antibodies, and in this way, reduced lung colonization and also protected mice against death. ClpP has been found to be highly immunogenic and conserved among different strains of S.

IL-6 is known to promote the proliferation of Th1 effector cells [49], and it is also involved in the differentiation of alloreactive Th1, but not alloreactive Th17, responses [50]. However, the role of IL-6 in driving the differentiation of Th17 effector cells is still a matter of debate [50, 51]. Neutralization of IL-6 or IL-23 partially inhibits Th17 differentiation induced by both C. albicans and S. aureus [44]. In our setting, IL-6 appeared to be dispensable for IL-17 induction, while it was partly involved in IL-22 production. The role played by

IL-1β released by PstS1-loaded DCs remains to be defined. Addition of a neutralizing anti-IL-1β Ab to the co-cultures caused a moderate inhibition MI-503 ic50 of IL-22 secretion by Ag85B-specific memory T cells, while it had no effects on either IFN-γ or IL-17 secretion. In addition, PstS1-stimulated selleck compound DCs might also activate Ag-independent memory T cells through signals mediated by MHC class II and co-stimulatory

molecules such as CD40, CD80, and CD86. These molecules, all upmodulated on DC surface by PstS1, are pivotal for the effector functions of memory T cells [52, 53] and for antigen-independent T-cell memory homeostasis [54]. In conclusion, our study defines a novel role for PstS1 in promoting the differentiation of unrelated Ag memory CD4+ T cells to produce IFN-γ, IL-17, and IL-22 via activation of CD8α− DCs. If properly administered, PstS1 may amplify protective Ag-specific memory responses in diverse TB vaccination settings while its neutralization may be considered to counteract excessive dangerous inflammation during advanced pulmonary TB. Overall, our findings may

greatly impact the design of novel vaccines as well Tacrolimus (FK506) as immunotherapeutic strategies in the management of TB. C57BL/6 and BALB/c mice (5–7 weeks old) were purchased from Charles River Laboratories. TLR2−/− (on a C57BL/6 background) mice were supplied by Dr. Carmen Fernandez. Mice were housed in a specific pathogen-free environment in animal facilities at the Istituto Superiore di Sanita. All procedures conducted on mice were in accordance with the conditions specified by the local Ethical Committee guidelines. All Mtb antigens were obtained from LIONEX Diagnostics and Therapeutics, Germany [26]. The endotoxin content (as measured by Limulus Amebocyte Lysate assay) was below 1 IU/μg protein, in a range of 0.048–0.087 IU/μg protein for different PstS1 batches, 0.022–0.035 IU/μg protein for different Ag85B batches, and 0.7 IU/μg protein for Ag85A. TT was a kind gift of Novartis (Siena, IT). Piceatannol was purchased from Calbiochem, dissolved in DMSO, and used at a 100 μM concentration. Neutralizing Abs to mouse IL-6 (eBioscience), to mouse IL-1β (Biolegend) and their isotype-matched controls were used at 5 μg/mL.

Other ways to prevent haemolysis include prescreening patients for active haemolysis, modifying the dose/rate regimen (for example, using the lowest effective dose, infusing slowly), pretreatment with steroids to reduce macrophage activation and increased INCB018424 manufacturer monitoring post-infusion. While IgG is well tolerated by the vast majority of patients, thromboembolic and haemolytic events can occur in some, and can be exacerbated by high doses and rapidity of infusion. Thrombotic events occur mainly in elderly patients with pre-existing

risk factors receiving i.v. infusions, and have been associated with activated clotting factors existing as contaminants in some IgG products. Trace haemolysis is fairly common but is rarely severe, and can usually be attributed to anti-A and/or anti-B isohaemagglutinins in the IgG product. Research is under way to identify risk factors for

these adverse events, and also ways to remove their causative components from the IgG product. F. A. B. would like to thank Meridian HealthComms Ltd for providing medical writing services. F. A. B. is a consultant for and participates in research sponsored by CSL Behring. He has participated in data safety monitoring boards related to IgG therapy for Octapharma and for the Chinese Green Cross (via the American Research Group). “
“Blastocystis LY2157299 mw is an intestinal protist found in many species including humans and pigs. It has a controversial pathogenesis and has been implicated as a potential cause of irritable bowel syndrome. Our previous studies identified pigs as potential animal models for blastocystosis by demonstrating that they were likely natural hosts of Blastocystis and can harbour subtypes (ST) in common with humans. Furthermore, our finding of a lack of intestinal histopathology associated with

Blastocystis infection in pigs is also a consistent finding in examined infected humans. In this study, we aimed to identify and characterize the Blastocystis-specific mucosal IgA response in pigs by immunoblotting, using pig faecal antibodies and Blastocystis antigen. why Faeces from 233 pigs representing three age groups (sows/boars, growers/weaners and piglets) and including five dexamethasone-immunosuppressed research pigs were tested. The majority (81·5%) of the pigs had faecal IgA reactivity against Blastocystis proteins of molecular weights of 17·5–120 kDa. Reactivity to a >250 kDa protein was found in 18·5% of pigs. Notably, immunosuppressed pigs and piglets were statistically more likely to have reactivity to this protein compared to growers/weaners and sows/boars, respectively. These results corroborate other findings suggesting that compromised immunity may predispose to blastocystosis and support our contention that pigs are potentially good models for pathogenesis studies.

These cells were isolated by cell sorting then cultured in the presence of IL-2, IL-7 or IL-15 without T-cell receptor stimulation (Fig. 6; see Supplementary Information, Figs S4 and S5). After 6 days, a population re-expressing CD45RA and down-modulating CD45RO emerged from the CD45RA− CD27+ cells cultured in the presence of IL-7 (Fig. 6a). T-cell receptor stimulation

alone did not induce CD45RA re-expression and neither did a panel of cytokines including transforming growth factor-β, IL-10 and IFN-α (unpublished observations). We also performed a CFSE dilution assay on CD45RA− CD27+ cells in the presence of IL-7 to assess whether CD45RA re-expression is accompanied by proliferation driven by IL-7. The CD45RA+ cells that were generated in vitro from CD45RA− CD27+ cells by IL-7 divided more than the cells that remained CD45RA− and CD45RO+ www.selleckchem.com/products/nivolumab.html in the same culture (Fig. 6b). Although a low level of CD45RA expression was observed in a small proportion of CD45RA− CD27+ CD4+ T cells that were cultured with IL-2 or IL-15 (see Supplementary Information, Fig. S4), this was considerably lower than that induced by IL-7 (Fig. 6a). The relatively

weak effect of IL-15 on the induction of CD45RA in CD45RA− CD27+ cells was not enhanced by a higher dose (10 ng/ml) of this cytokine (data not shown). The CD45RA− CD27− subset cultured in the same experimental conditions did respond to IL-7 in terms of survival (data not shown) but did not re-express CD45RA and remained CD45RO+ throughout the culture period (see Supplementary Information,

Fig. S5). These results suggest that IL-7-driven homeostatic proliferation Tyrosine Kinase Inhibitor Library can induce the re-expression of CD45RA in CD45RA− CD27+ CD4+ T cells but Celecoxib cannot induce the CD45RA− CD27− population to form the CD45RA+ memory population. We next determined whether the memory CD45RA+ cells that were generated in vitro resembled phenotypically those that are found in vivo. To do this we monitored the expression of CD27, Bcl-2 and IL-7Rα after different time-points of IL-7 treatment of CD45RA− CD27+ CD4+ T cells in vitro. The population that remained CD45RA− CD45RO+ expressed homogeneously high levels of Bcl-2 and IL-7Rα throughout the culture period (Fig. 6c), except for the initial down-regulation of IL-7Rα (visible at day 5). In contrast the population of CD45RA+ cells that emerged down-regulated both Bcl-2 and IL7-Rα over time (Fig. 6c). Interleukin-7 stimulation of CD45RA− CD27+ CD4+ T cells results in the generation of a population with heterogeneous expression of CD27. However, a small percentage of the CD45RA re-expressing cells are CD27− (see Supplementary Information, Fig. S6). As IL-7 induces CD45RA but not complete loss of CD27 in the timeframe of experimental protocol we acknowledge that other factors in addition to IL-7 may also be required for the generation of a CD45RA+ CD27− T-cell population from CD45RA− CD27+ cells.

An amount of 0·1 g of the faecal specimens from each of the groups at 0 day (day before C. parvum infection) and daily for 13 days following infection was weighed and purified through discontinuous sucrose gradients (13). Then, 10 μL of the purified faecal matter was taken to make a smear on glass slide. The slides were air dried,

stained with modified acid-fast HM781-36B staining method and examined for Cryptosporidium oocysts with microscope. Cryptosporidium parvum was counted in the entire smear using a 20× objective by a blinded observer. The results were expressed as number of C. parvum/g of faeces. Results of serological assays, production of cytokines and faecal oocyst shedding after C. parvum challenge were compared using analysis of variance (anova) and t-test using the spss software. A P-value of <0·05 was considered different. To study the capacity of multivalent peptides in stimulating immune responses and protecting host from C. parvum infection, first we generated the monovalent peptide fragment rCp23 and divalent

peptide rCp15–23 through recombinant DNA techniques. To identify buy PF-02341066 these cloned genes, the plasmid constructs were sequenced and analysed by BLAST searching. As in Figure 2a, the sequences we obtained are identical to Cp23 and Cp15 genes of C. parvum reported previously (15). To determine further whether the cloned genes can generate expected peptide, immunoblotting was performed using the sera from rabbits experimentally

infected with C. parvum. The Adenosine triphosphate bands appeared at 27 and 46 kDa position indicated that the sizes of the peptides were the same as estimated molecular weights (Figure 2b). To examine the antigen specificity of the proteins, rCp15–23, rCp23 or crude extract of C. parvum was used to coat 96-well plate and reacted with sera from rabbits experimentally infected with C. parvum oocysts. We found that all of the three antigens had higher specific immune reaction with the sera and the immune response using rCp15–23 generated stronger reaction than that in either rCp23 or crude extract group (Figure 3). Immunization of BALB/c mice three times with 10 μg of the proteins at 2-week intervals resulted in the generation of specific antibody responses against rCp23 protein, crude extract of C. parvum and rCp15–23 fusion protein (Figure 4). The concentrations of IgG remained at low levels until days 14 after the first vaccination, whereas the second dose of vaccine rapidly and significantly boosted the responses with the titre at 1 : 22 810 for rCp23 and 1 : 81 280 for rCp15–23. A peak concentration was observed after third boost (with the titre of 1 : 51 200 for rCp23 and 1 : 102 400 for rCp15–23). The vaccination of the mice with both the recombinant Cp15–23 fusion protein and rCp23 induced stronger antibody response than crude extract (P < 0·05).