Anti-osteosarcoma effect of antiserum against cross antigen TPD52 between osteosarcoma and Trichinella spiralis.

BACKGROUND: Trichinella spiralis (T. spiralis) is a parasite occurring worldwide that has been proven to have antitumour ability. However, studies on the antitumour effects of cross antigens between the tumour and T. spiralis or antibodies against cross antigens between tumours and T. spiralis are rare. METHODS: To study the role of cross antigens between osteosarcoma and T. spiralis, we first screened the cDNA expression library of T. spiralis muscle larvae to obtain the cross antigen gene tumour protein D52 (TPD52), and prepared fusion protein TPD52 and its antiserum. The anti-osteosarcoma effect of the anti-TPD52 antiserum was studied using cell proliferation and cytotoxicity assays as well as in vivo animal models; preliminary data on the mechanism were obtained using western blot and immunohistochemistry analyses. RESULTS: Our results indicated that TPD52 was mainly localized in the cytoplasm of MG-63 cells. Anti-TPD52 antiserum inhibited the proliferation of MG-63 cells and the growth of osteosarcoma in a dose-dependent manner. The tumour inhibition rate in the 100 µg treatment group was 61.95%. Enzyme-linked immunosorbent assay showed that injection of anti-TPD52 antiserum increased the serum levels of IFN-γ, TNF-α, and IL-12 in nude mice. Haematoxylin and eosin staining showed that anti-TPD52 antiserum did not cause significant pathological damage. Apoptosis of osteosarcoma cells was induced by anti-TPD52 antiserum in vivo and in vitro. CONCLUSIONS: Anti-TPD52 antiserum exerts an anti-osteosarcoma effect by inducing apoptosis without causing histopathological damage.

A cross-reactive monoclonal antibody to nematode haemoglobin enhances protective immune responses to Nippostrongylus brasiliensis.

BACKGROUND: Nematode secreted haemoglobins have unusually high affinity for oxygen and possess nitric oxide deoxygenase, and catalase activity thought to be important in protection against host immune responses to infection. In this study, we generated a monoclonal antibody (48Eg) against haemoglobin of the nematode Anisakis pegreffii, and aimed to characterize cross-reactivity of 4E8g against haemoglobins of different nematodes and its potential to mediate protective immunity against a murine hookworm infection. METHODOLOGY/PRINCIPAL FINDINGS: Immunoprecipitation was used to isolate the 4E8g-binding antigen in Anisakis and Ascaris extracts, which were identified as haemoglobins by peptide mass fingerprinting and MS/MS. Immunological cross-reactivity was also demonstrated with haemoglobin of the rodent hookworm N. brasiliensis. Immunogenicity of nematode haemoglobin in mice and humans was tested by immunoblotting. Anisakis haemoglobin was recognized by IgG and IgE antibodies of Anisakis-infected mice, while Ascaris haemoglobin was recognized by IgG but not IgE antibodies in mouse and human sera. Sequencing of Anisakis haemoglobin revealed high similarity to haemoglobin of a related marine nematode, Psuedoterranova decipiens, which lacks the four -HKEE repeats of Ascaris haemoglobin important in octamer assembly. The localization of haemoglobin in the different parasites was examined by immunohistochemistry and associated with the excretory-secretary ducts in Anisakis, Ascaris and N. brasiliensis. Anisakis haemoglobin was strongly expressed in the L3 stage, unlike Ascaris haemoglobin, which is reportedly mainly expressed in adult worms. Passive immunization of mice with 4E8g prior to infection with N. brasiliensis enhanced protective Th2 immunity and led to a significant decrease in worm burdens. CONCLUSION: The monoclonal antibody 4E8g targets haemoglobin in broadly equivalent anatomical locations in parasitic nematodes and enhances host immunity to a hookworm infection.

Passive immunization with a monoclonal IgM antibody specific for Strongyloides ratti HSP60 protects mice against challenge infection.

It is estimated that 30-100 million people are infected with the pathogenic nematode Strongyloides stercoralis worldwide but parasite control is still based on anti-helminthic treatment. To develop protective vaccination strategies, we use the murine model of Strongyloides ratti infection. We have shown recently that vaccination with alum-precipitated, but not with native or CFA-emulsified S. ratti heat shock protein 60 (srHSP60) conferred protection to challenge infection. Here we describe the generation of a monoclonal IgM specific for srHSP60. Anti-srHSP60 detected human and srHSP60 and stained S. ratti infective larvae in vitro. Passive immunization of mice with monoclonal anti-srHSP60 IgM led to reduced numbers of migrating larvae in lung and head, reduced numbers of parasitic adults in the small intestine and reduced larval output upon S. ratti challenge infection. Taken together, our findings highlight the relevance of srHSP60 as vaccine candidate for the induction of antibody-mediated protection against Strongyloides infection.

Monoclonal antibody 12D5 inhibits eosinophil infiltration in the brain of Angiostrongylus cantonensis-infected BALB/c mice.

Each of BALB/c mice was infected with 50 Angiostrongylus cantonensis larvae. One group of mice received an intraperitoneal injection of 50 µg 12D5 monoclonal antibody (mAb) against a 98 kDa antigen of adult worms at 10 days post-infection (dpi), with a booster injection of 25 µg at 12 dpi. Five mice from each group were sacrificed at 14 dpi for pathological examination and RNA extraction. The infiltration of eosinophils and severity of eosinophilic meningitis were reduced in 12D5 mAb-treated mice compared with the infected mice without 12D5 treatment. The levels of eotaxin mRNA expression in spleen significantly increased and the expression of the Th2-type cytokine IL-5 significantly decreased. However, the expression of IL-4 was not changed. 12D5 mAb can observably enhance the survival rate of infected mice and reduce symptoms of angiostrongyliasis. A. cantonensis infection is a major cause of eosinophilic meningoencephalitis. The results of this study could be helpful for the development of treatment of human angiostrongylosis.

An enzymatically inactivated hemoglobinase from Necator americanus induces neutralizing antibodies against multiple hookworm species and protects dogs against heterologous hookworm infection.

Hookworms digest hemoglobin from erythrocytes via a proteolytic cascade that begins with the aspartic protease, APR-1. Ac-APR-1 from the dog hookworm, Ancylostoma caninum, protects dogs against hookworm infection via antibodies that neutralize enzymatic activity and interrupt blood-feeding. Toward developing a human hookworm vaccine, we expressed both wild-type (Na-APR-1(wt)) and mutant (Na-APR-1(mut)-mutagenesis of the catalytic aspartic acids) forms of Na-APR-1 from the human hookworm, Necator americanus. Refolded Na-APR-1(wt) was catalytically active, and Na-APR-1(mut) was catalytically inactive but still bound substrates. Vaccination of canines with Na-APR-1(mut) and heterologous challenge with A. caninum resulted in significantly reduced parasite egg burdens (P=0.034) and weight loss (P=0.022). Vaccinated dogs also had less gut pathology, fewer adult worms, and reduced blood loss compared to controls but these did not reach statistical significance. Vaccination with Na-APR-1(mut) induced antibodies that bound the native enzyme in the parasite gut and neutralized enzymatic activity of Na-APR-1(wt) and APR-1 orthologues from three other hookworm species that infect humans. IgG1 against Na-APR-1(mut) was the most prominently detected antibody in sera from people resident in high-transmission areas for N. americanus, indicating that natural boosting may occur in exposed humans. Na-APR-1(mut) is now a lead antigen for the development of an antihematophagy vaccine for human hookworm disease.

Effect of CD4+ T lymphocyte depletion on resistance of Gulf Coast Native lambs to Haemonchus contortus infection.

It has been reported that CD4(+) T lymphocytes are important in acquired immunity to gastrointestinal nematode infection. Whether these lymphocytes are also involved in the immune response of naturally resistant Gulf Coast Native (GCN) sheep to Haemonchus contortus infection remains to be defined. The objective of this study was to determine the role of CD4(+) T lymphocytes in this resistance. Ten GCN lambs were randomly assigned to a control (n=5) or a treatment (n=5) group. The treatment consisted of a series of IV injections with mouse anti-ovine CD4(+) T lymphocyte monoclonal antibodies for a period of 3 weeks. After the second treatment, all lambs were experimentally infected with 10,000 H. contortus infective larvae by oral inoculation. All lambs were monitored for fecal egg counts, blood packed cell volumes, white blood cell differential counts and serum antibody responses on a weekly basis. Fluorescence-activated cell sorter (FACS) analysis was done biweekly to enumerate CD4(+) T lymphocytes in peripheral blood. Necropsies were performed at the end of the study and 10% of the contents of the gastrointestinal tract were preserved for nematode enumeration and identification. Also at necropsy, mesenteric lymph nodes were extracted and FACS analysis was run on lymphoid cells. Mean fecal egg counts on day 21 and 28 post-infection and nematode counts at necropsy of the treated group were significantly (p<0.05) higher than that of the control group. Percent CD4(+) T lymphocytes in peripheral blood was significantly (p<0.05) lower in the treatment group than in the control group from day 9 to the end of the study. No differences were found in blood packed cell volumes, white blood cell differential counts, antibody titer or lymph node CD4(+) lymphocytes between groups. Lambs depleted of their CD4(+) T lymphocytes were more susceptible to H. contortus infection than undepleted lambs. The results of this study suggest that CD4(+) T lymphocytes are associated with the natural resistance of GCN sheep to H. contortus infection.

Passive protection against fasciolosis in mice by immunization with a monoclonal antibody (ES-78 MoAb).

Recently, we reported a partial characterization of the epitope recognized by the ES-78 monoclonal antibody (MoAb). This monoclonal antibody was obtained from spleen lymphocytes of a mouse immunized with excretory-secretory antigens of Fasciola hepatica adult worms. In the present study, we report the results obtained in experiments of passive protection using this MoAb in BALB/c mice infected with 15 Fasciola hepatica metacercariae. The monoclonal antibody was able to reduce the parasite burden when administered 24 h before challenge but not when delivered 7 days after challenge. The antibody recognition of digestive tract structures in 3-week-old parasites was demonstrated by immune histochemical techniques. The antigens purified by affinity chromatography using this antibody had molecular weights of 14-20, 25-29 and 36-45 kDa and demonstrated proteinase activity similar to cathepsin L. These results suggest that the antigens carrying the epitope recognized by the ES-78 MoAb may be used as target in the protection against fasciolosis.

The crucial role of granulocytes in the early host defense against Strongyloides ratti infection in mice.

The involvement of granulocytes in the host early defense against the nematode, Strongyloides ratti, was studied. It was confirmed that granulocytes were effectively depleted for 4 days by anti-granulocyte monoclonal antibody (anti-Gr-1). To examine the involvement of granulocytes in the host defense against migrating larvae, 2,000 S. ratti infective larvae (L3) were inoculated subcutaneously 1 day after antibody treatment. The number of S. ratti eggs secreted in feces (EPG) was higher in the granulocyte-depleted group than in the control group. The number of migrating larvae also increased in the granulocyte-depleted group in accordance with the increase in EPG. Therefore granulocytes are crucial for the host early defense against migrating larvae of S. ratti. Next, the involvement of granulocytes in the intestinal early defense was examined. Mice were treated with the antibody on day 3 post-infection. On that day, almost all inoculated larvae reached the intestine and molted to become adults. EPG on day 5 post-infection was increased by the antibody treatment, but no effect was observed on intestinal worm numbers. The fecundity (EPG/worm number) of S. ratti adult worms in the granulocyte-depleted group was higher than that in the control group. Thus granulocytes are also involved in the intestinal early defense through suppressing fecundity of the adult worms. On the other hand, the depletion of granulocytes had no effect on the late adaptive response against S. ratti adult worms (e.g. number of intestinal mucosal mast cells, time of worm expulsion). These results suggest that granulocytes are mainly involved in the host early defense against parasites.

Neonatal idiotypic exposure alters subsequent cytokine, pathology, and survival patterns in experimental Schistosoma mansoni infections.

Exposure to maternal idiotypes (Ids) or antigens might predispose a child to develop an immunoregulated, asymptomatic clinical presentation of schistosomiasis. We have used an experimental murine system to address the role of Ids in this immunoregulation. Sera from mice with 8-wk Schistosoma mansoni infection, chronic (20-wk infection) moderate splenomegaly syndrome (MSS), or chronic hypersplenomegaly syndrome (HSS) were passed over an S. mansoni soluble egg antigen (SEA) immunoaffinity column to prepare Ids (8WkId, MSS Id, HSS Id). Newborn mice were injected with 8WkId, MSS Id, HSS Id, or normal mouse immunoglobulin (NoMoIgG) and infected with S. mansoni 8 wk later. Mice exposed to 8WkId or MSS Id as newborns had prolonged survival and decreased morbidity compared with mice that received HSS Id or NoMoIgG. When stimulated with SEA, 8WkId, or MSS Id, spleen cells from mice neonatally injected with 8WkId or MSS Id produced more interferon gamma than spleen cells from mice neonatally injected with HSS Id or NoMoIgG. Furthermore, neonatal exposure to 8WkId or MSS Id, but not NoMoIgG or HSS Id, led to significantly smaller granuloma size and lower hepatic fibrosis levels in infected mice. Together, these results indicate that perinatal exposure to appropriate anti-SEA Ids induces long-term effects on survival, pathology, and immune response patterns in mice subsequently infected with S. mansoni.

A trial to enhance the efficiency of Cyclosporin A in the treatment of Schistosoma mansoni infection by immunization of mice.

Cyclosporin A (CsA) acts in two distinct modes against Schistosoma mansoni (S. mansoni) infection. It behaves in part as an antihelminthic and also as an immunomodulator. In this study, two methods were performed to increase the efficacy of the subcurative dose of CsA (30 mg/kg). These methods were, passive immunization where the drug was given simultaneously with rabbit antisera post infection and active immunization where the worm surface antigen was given prior to infection. The results showed that both methods led to enhancement of the curative effect of the CsA. However, the active immunization gave more significant reduction in liver worm and egg loads. Histopathological study showed small size and few number of hepatic granulomas in the passively immunized group while in the active group, there was just few and small collection of inflammatory cells. Moreover, the indirect fluorescent antibody test visualized damage to the worm tegument in both types of immunization. Thus, it could be concluded that active immunization increased the immunomodulatory effect of CsA in treatment of S. mansoni with less toxic effects by using a subcurative dose.

Temporal differences in praziquantel- and oxamniquine-induced tegumental damage to adult Schistosoma mansoni: implications for drug-antibody synergy.

A temporal study of the effects on the tegument of Schistosoma mansoni adult worm following in vivo praziquantel and oxamniquine treatment was performed. Drug-induced damage to the tegument, exposure of surface antigens and attachment of host antibody occurred rapidly, within 1 h, following praziquantel treatment. Oxamniquine-treated worms required 4-8 days for these effects to be apparent. The 2 drugs differed in the degree and sites of damage on the worm surface. The administration of 2 different polyspecific rabbit sera with drug significantly increased the efficacy of praziquantel when administered with the drug, but not when given 6-9 days after drug treatment. In contrast, only 1 serum was synergistic with oxamniquine when administered with drug and both sera were synergistic when given 6-9 days after drug treatment. The effect of immune killing of drug-treated worms is discussed.

Protection of mice against Schistosoma mansoni infection by passive transfer of sera from infected rabbits.

Sera from rabbits infected with unattenuated Schistosoma mansoni cercariae conferred significant levels of protection against S. mansoni challenge (P < 0.001) after passive transfer to mice. Infected rabbit sera were only effective in conferring protection when transferred during the first week of infection, and were not effective when administered against liver-stage worms. Immunoglobulins isolated from the infected rabbit sera with Protein A-Sepharose were shown to be responsible for the transfer of protection to mice. Immunofluorescence studies demonstrated that the sera were more reactive against the surface of three hour-old mechanically transformed schistosomula than against the surfaces of lung-stage schistosomula. The sera from infected rabbits reacted polyspecifically against antigens in cercaria, schistosomula, and the worm and egg stages of the S. mansoni life-cycle. The host parasite relationship of S. mansoni in the rabbit is discussed.

Protective immunisation of guinea pigs against Dictyocaulus viviparus using excretory/secretory products of adult parasites.

Parasite preparations were examined for their ability to induce protective immunity against Dictyocaulus viviparus in guinea pigs. Dunkin-Hartley strain guinea pigs were immunised with somatic extracts of adult parasites, somatic extracts of third stage larvae or excretory/secretory (ES) products from adult parasites. The groups were immunised twice with Freund's adjuvant four weeks apart and challenged with 6000 infective L3. Significant levels of protective immunity were observed only in the adult ES-immunised animals. The antibody responses of the different groups were compared following analysis by ELISA and immunoprecipitation. To examine the protective role of antibody, guinea pigs were passively immunised with serum from animals immunised with adult ES products or serum from guinea pigs exposed to experimental D. viviparus infection. Following challenge with infective L3, lung-worm burdens of these groups were significantly lower than in guinea pigs which received normal sera. The results suggest that D. viviparus adult ES products contain protective antigens and that antibody-mediated mechanisms contribute to immune protection.

Immune dependence of schistosomicidal chemotherapy: an ultrastructural study of Schistosoma mansoni adult worms exposed to praziquantel and immune serum in vivo.

This study examines the immune-dependence of praziquantel (PZQ) for the treatment of Schistosomiasis mansoni in mice. We have shown elsewhere from worm recovery data that the efficacy of PZQ is significantly enhanced when mice are treated concomitantly with antisera raised against antigens released from adult schistosomes, even though such antisera show no intrinsic helminthotoxic activity (Doenhoff et al. 1987, Doenhoff, Modha & Lambertucci 1988). Moreover, indirect immunofluorescence assays have shown that male worms exposed to the dual treatment regime in vivo bind antiserum to their dorsal surfaces in a pattern that seems to follow the outline of the dorsal tubercles. Scanning and transmission electron microscopy have now been used to further define the features of damage inflicted upon worms through exposure to antiserum alone, drug alone, or the two treatments in combination. Such investigations revealed that the antiserum induces a classical membrane repair process in worms of both sexes, but little other damage. PZQ causes the formation of spherical protuberances on the dorsal tubercles of male worms, while the dual treatment regime induces both kinds of damage in male schistosomes, but with much enhanced severity. The protuberances show evidence of explosion and some regions of the tegument become completely destroyed. Regions other than the dorsal surfaces of the male worms do not exhibit comparable trauma, and neither do the females. These data are discussed in relation to the known schistosomicidal activity of PZQ, the notion that male and female worms exhibit regional and sexual differences in susceptibility, documented evasive strategies of the parasite and the interdependence of immuno- and chemotherapy.

Protective immunity against Brugia malayi infective larvae in mice. II. Induction by a T cell-dependent antigen isolated by monoclonal antibody affinity chromatography and SDS-PAGE.

A mAb directed against filarial worm secretory/excretory product and reactive with Brugia malayi larval worm surface was used in conjunction with preparative SDS-PAGE to isolate protective Ag from extracts of adult B. malayi. The IgM mAb OVH bound to a repeating carbohydrate epitope present in adult, infective, and fourth stage larvae and microfilariae of B. malayi, and on the surface of fourth stage larvae. Ag bearing this epitope were also present in the sera of hosts infected with a variety of helminths, including Brugia, Onchocerca, Dirofilaria, and Paragonimus. Affinity chromatography of SDS extract of adult Brugia, using mAb OVH immobilized on agarose beads, isolated several Ag that separated into multiple protein staining bands on SDS-PAGE. In comparing SDS-PAGE-fractionated Ag from the crude SDS extract with fractionated mAb OVH-isolated Ag for the ability to protect BALB/c mice from challenge with B. malayi-infective larvae, it was found that of the mAb OVH-isolated Ag only those at a molecular mass of 26 to 32 kDa were protective while the original SDS extract yielded protective Ag at the following molecular mass: greater than 200, 170 to 200, 40 to 44, 33 to 36, 23 to 28, 20 to 22, and 17 to 19 kDa. Although Ag isolated by mAb OVH were highly protective, they failed to induce high antibody levels against the immunogen or SDS extracts compared to crude SDS extract immunized mouse sera, as determined by immunoblot and ELISA. Transfer of nylon wool non-adherent T cells from BALB/c mice immunized with the 26- to 28-kDa fraction of mAb OVH-isolated Ag to naive mice just before challenge with infective larvae of B. malayi resulted in a 70% reduction in larvae recovered 14 days after challenge.

Immune responses during human schistosomiasis mansoni. XVI. Idiotypic differences in antibody preparations from patients with different clinical forms of infection.

Antibodies were purified from pooled sera from patients with different clinical forms of schistosomiasis mansoni on immunoaffinity columns of schistosome soluble egg Ag (SEA). As previously reported, T lymphocytes in PBMC preparations from schistosomiasis patients (but not control subjects who have never been infected) proliferate when cultured in the presence of certain of these anti-SEA purified antibodies. We now show that PBMC from most patients with chronic schistosomiasis, regardless of the clinical form of their infection, respond to anti-SEA antibodies from sera of asymptomatic (intestinal) or hepatointestinal patients. In stark contrast, none responds to anti-SEA antibodies purified from sera of acute or hepatosplenic patients. All of these multiclonal anti-SEA antibody preparations were active in anti-SEA ELISA assays and gave comparable patterns of reactivity with SEA upon immunoblotting analysis. Immunization of rabbits with some of these anti-SEA antibody preparations, followed by absorption of the rabbit antisera on absorbents of normal Ig, produced specific anti-Id reagents. Use of these reagents in competitive ELISA systems demonstrated that the Id in stimulatory and nonstimulatory anti-SEA antibody preparations differ with regard to the proportion of the serologically defined Id expressed by each. It appears possible to screen patients' plasmas for the presence of shared Id by use of suitable Id/anti-Id competitive ELISA assays. Taken together these data indicate that only certain Id-positive preparations are stimulatory to patients' PBMC, and the expression of these T cell stimulatory, immunoregulatory Id on anti-SEA antibodies correlates with the clinical form of a patient's infection.

Protective immunity in mice vaccinated with the Schistosoma mansoni P-28-1 antigen.

The P28-1 Ag induces a strong protective immunity toward Schistosoma mansoni infection in various experimental models. T lymphocytes of mice immunized with the recombinant P28-1 Ag were stimulated in vitro by schistosome Ag of different development stages and by three P28-1 Ag-derived synthetic peptides. The most significant stimulation was achieved with the 24-43 peptide. The use of two fragments of this peptide showed that the P28-1 T lymphocyte specificity concerned essentially the NH2 terminal sequence of the 24-43 peptide. Moreover, T lymphocytes specific for the 24-43 peptide were stimulated by both schistosome Ag and the recombinant P28-1 protein. The passive transfer of (Th + Ts) lymphocytes recovered from P28-1 Ag-immunized mice increased the IgG response to P28-1 and its peptides during infection but did not protect against a challenge infection, such as the passive transfer of anti-P28-1 sera. In contrast, P28-1 specific Th cell lines maintained in culture for 2 mo, passively transferred a strong protection (50%) to infected mice. Supernatants of P28-1-specific T cells obtained after stimulation with the corresponding Ag, were able to confer cytotoxic properties to platelets and macrophages. The presence of IFN-gamma for the cytotoxicity mediated by platelets and macrophage activating factor for the cytotoxicity mediated by macrophages in these supernatants is in a large part responsible for the parasite killing observed. Finally, a preliminary immunogenetic approach with H-2 congenic mice on BALB background showed that the P28-1 Ag T cell response was under the control of the MHC and that the H-2b haplotype determined a low response to P28-1 Ag and its peptides while H-2d and k haplotypes determined high responders.

Cytotoxic effects in vitro of human monocytes and macrophages on schistosomula of Schistosoma mansoni.

Human peripheral blood monocytes from normal donors were isolated by differential centrifugation and cultured in vitro in hydrophobic Teflon-coated tissue culture bags. Cells were harvested between 0 and 10 days and tested for their ability to kill schistosomula of Schistosoma mansoni in an in-vitro cytotoxicity assay. Freshly isolated, unstimulated monocytes demonstrated minimal cytotoxic capability. However, this was increased if the cells were pretreated with human recombinant gamma interferon (IFN-gamma), or with specific anti-S. mansoni antiserum. As the monocytes matured in vitro there were marked increases in the levels of antibody-independent killing of schistosomula. Monocytes grown in vitro with IFN-gamma (10(4) u/ml) took 2-3 days to develop almost maximal cytotoxicity (mean 94% kill of schistosomula). In contrast, unstimulated monocytes (no IFN-gamma) took between 5 and 7 days to achieve comparable cytotoxicity (mean 99% kill). Killing of the schistosomula was dependent upon a high effector to target ratio, and was a relatively slow phenomenon in vitro, parasite attrition occurring between 17 and 36 h. Supernatants from cytotoxic macrophages were ineffective in mediating cytotoxicity of the parasite.

Role of a mouse monoclonal IgE antibody in passive transfer of immunity to Schistosoma japonicum infection.

We have been able to produce a mouse monoclonal IgE antibody specific to an adult worm antigen extracted from Schistosoma japonicum (Sj). The antibody was able to elicit passive cutaneous anaphylaxis in the rat skin against Sj with the highest titer of 1:256,000 but did not cross-react with S. mansoni antigen. The antibody recognized a 97-kDa molecule expressed on the surface of mechanically transformed schistosoma of S. japonicum. Passive transfer of the antibody into mice in the early stage of challenge infection resulted in a partial but significant reduction of recovery of adult worms. Induction of eosinophilia by an oral administration of embryonated eggs of Toxocara canis prior to challenge infection enhanced the reduction.

Role of a mouse monoclonal IgE antibody in passive transfer of immunity to Schistosoma japonicum infection

We have been able to produce a mouse monoclonal IgE antibody specific to an adult worm antigen extracted from Schistosoma japonicum (Sj). The antibody was able to elicit passive cutaneous anaphylaxis in the rat skin against Sj with the highest titer of 1:256,000 but did not cross-react with S. mansoni antigen. The antibody recognized a 97-kDa molecule expressed on the surface of mechanically transformed schistosoma of S. japonicum. Passive transfer of the antibody into mice in the early stage of challenge infection resulted in a partial but significant reduction of recovery of adult worms. Induction of eosinophilia by an oral administration of embryonated eggs of Toxocara canis prior to challenge infection enhanced the reduction.