The acquisition and loss of antigen-specific cellular immune responsiveness in acute and chronic schistosomiasis in man.
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To characterize the development and evolution of cellular immune responsiveness in individuals infected with the parasite Schistosoma mansoni, we studied fifteen patients with acute, subacute and chronic schistosomiasis. Lymphocytes from the three acutely infected patients responded vigorously to schistosome antigens in an in vitro blastogenic assay. By contrast, cells from nine chronically infected individuals were essentially unreactive to these same antigens. Patients infected for an intermediate period of time (9 months) generated responses between those of acute and chronic patients. The diminished responsiveness of chronically infected individuals was specific for schistosome antigens and did not extend to humoral immune responses. Following treatment of the infection with niridazole, these patients temporarily regained responsiveness to schistosome antigens. From these data we speculate that during the course of this parasitic helminth infection there develops a progressive and specific modulation of antigen recognition and proliferation by lymphocytes to schistosome antigens, and that such diminished immune reactivity may be important in maintaining the unique biological relationship which exists between a host and its parasites.Keywords:
Schistosoma
Niridazole
Cellular immunity
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Schistosoma mansoni adult worm antigens were tested for cross-reactions with sera obtained from patients infected with S. japonicum. The sera consistently recognized a doublet of bands, in immunoblots, which had molecular weights of approximately 31 and 32 kilodaltons (kD). This reaction was found to be markedly reduced with sera of patients who had received chemotherapy and who had a low risk of reinfection. Sera obtained from uninfected persons or from patients infected with other parasites never reacted with the antigen doublet. Schistosoma japonicum-infected mice produced antibodies during prepatency which predominantly recognized antigens of this molecular weight range in immunoblots performed with S. mansoni or S. japonicum proteins. Sera from S. mansoni-infected patients with a high specificity for the diagnostic S. mansoni-antigen cross-reacted with a corresponding component also in S. japonicum worms. Immunofluorescence assays performed with sera of schistosomiasis japonica patients confirmed earlier results localizing the diagnostic 31/32 kD antigens in the gut of S. mansoni. These cross-reacting 31/32 kD S. mansoni protein antigens may be applied for the immunodiagnosis of schistosomiasis japonica.
SCHISTOSOMIASIS JAPONICA
Schistosoma
Immunofluorescence
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We investigated the type and strength of the immune response to schistosome antigens in a group of 20 Dutch travelers who had been infected with Schistosoma spp. during a group visit to Mali in 1991 and 8 non-infected controls. At the time, 9 had Katayama syndrome (KS), and 11 remained asymptomatic. All had been treated with praziquantel. Eight years later, serology remained positive in all 20 formerly infected travelers. The lymphocyte proliferative responses and cytokine responses (interleukin 13 [IL-13], IL-10, and interferon [IFN-γ] responses to soluble egg antigens and the IL-13, IL-10, and IL-5 response to adult worm antigen) were stronger in the travelers than in the controls and tended to be stronger in those with KS compared with those who had remained asymptomatic. In conclusion, Schistosoma infection induced a memory immune response, and people who experienced KS tended to have a stronger immune response to schistosome antigens than their asymptomatic counterparts.
Schistosoma
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Immunological reactivity in 10 rhesus monkeys was monitored over a 22-week period. Cellular and humoral responses of three animals were studied after primary infection with Schistosoma mansoni. Two uninfected animals served as controls. Increased lymphocyte proliferative responsiveness to mitogens and adult worm antigen was evident during the prepatent period of the infection. Marked suppression of these responses occurred during the acute phase of the disease, but by weeks 9 and 11 the animals were again responsive to mitogens and antigen, respectively, and remained so throughout the remainder of the observation period. No antibody response to various cercarial, adult worm, and egg antigens could be detected until weeks 5 to 7, after which these responses also persisted. Comparison of the immunological reactivities of these animals with primary infection and those of five chronically infected immune animals indicated possible correlations between protective immunity and (i) strong Cercarienhüllenreaktion reactivity, and (ii) lymphocyte proliferative responsiveness to adult worm antigen.
Cellular immunity
Humoral immunity
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SUMMARY Early diagnosis is important when handling patients with acute schistosomiasis. This state is usually more severe in travellers and tourists than in the immune, resident patients. With increased travelling to areas endemic for schistosomiasis, a tool is needed to solve the problem of differential diagnosis due to the non-specific symptoms of the early stages of the disease. Early appearance of antibodies against excretory/secretory antigens of the intestinal tract in the adult worm was seen in six individuals recently infected with Schistosoma mansoni, using an indirect immunofluorescence technique. The antibodies were of IgM, IgG and IgA classes, and of the IgG1, IgG3 and IgA1 subclasses as detected by ELISA using an antigen preparation of adult worm. On immunoblots, using a freeze-dried adult worm antigen, IgG1 and IgG3 antibodies recognized antigens of 32–35 kD. Antibodies against these antigens could thus be a marker of early infection in previously non exposed visitors to endemic areas.
Immunofluorescence
Schistosoma
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Circulating schistosome antigens (CSA), circulating immune complexes (CIC) and C3 breakdown product - C3d - were investigated in human schistosomiasis in comparison to the S. mansoni egg count. A close relationship was observed between the mean number of eggs/g of stool and the detection of CSA (evaluated by the radioimmunoprecipitation-PEG assay - Ripega), CIC (Clq-binding test) and C3d levels (quantitated by radial immunodiffusion). All the patients with more than 500 S. mansoni eggs/g of stool also presented antigen '4', specific of the genus Schistosoma, in the serum. A significant correlation was noticed between levels of CSA and CIC. This suggests the involvement of several schistosome antigens in the detected CIC. No relationship was noted between CIC and C3d levels. In contrast, there was a highly significant correlation between levels of CSA and C3d. The interaction between certain schistosome antigens and the complement system is discussed.
Schistosoma
Immunodiffusion
Radial immunodiffusion
Complement fixation test
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Diagnosis of schistosomiasis still depends upon demonstration of eggs in excreta, by which time significant pathology may occur to the human host. This study was undertaken to identify Schistosoma mansoni antigen(s) to be exploited in serodiagnosis of prepatent and/or acute infections. Immunoglobulin G and M responses of inbred and outbed mice to Schistosoma mansoni whole adult worm antigen were monitored in immunoblots using sera obtained at sequential times from mice infected with either 600 or 100 Schistosoma mansoni cercariae each. Regardless of the initial infection dose, immunoblot reactions to two doublets, 31/32 and 34/35 kDa appeared as early as two and three weeks post infection respectively and reactions to 38 and 70 kDa antigens appeared after five weeks infection. Antigens 31/32 and 38 induced both IgG and IgM responses whereas 34/35 and 70 predominantly induced IgG response. Homologues of these four antigens equally reactive with serum of infected mice were also demonstrated in Schistosoma haematobium, worms. Examination of sera from 25 patients suffering from acute Schistosoma mansoni, two suffering from Schistosoma haematobium and 16 patients suffering from infections with other parasite species confirmed the potential of 31/32, 34/35 and 38 kDa antigens in the specific diagnosis of prepatent and acute schistosomal infections but showed cross-reactivity of the 70 kDa antigen.
Schistosoma
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To characterize the development and evolution of cellular immune responsiveness in individuals infected with the parasite Schistosoma mansoni, we studied fifteen patients with acute, subacute and chronic schistosomiasis. Lymphocytes from the three acutely infected patients responded vigorously to schistosome antigens in an in vitro blastogenic assay. By contrast, cells from nine chronically infected individuals were essentially unreactive to these same antigens. Patients infected for an intermediate period of time (9 months) generated responses between those of acute and chronic patients. The diminished responsiveness of chronically infected individuals was specific for schistosome antigens and did not extend to humoral immune responses. Following treatment of the infection with niridazole, these patients temporarily regained responsiveness to schistosome antigens. From these data we speculate that during the course of this parasitic helminth infection there develops a progressive and specific modulation of antigen recognition and proliferation by lymphocytes to schistosome antigens, and that such diminished immune reactivity may be important in maintaining the unique biological relationship which exists between a host and its parasites.
Schistosoma
Niridazole
Cellular immunity
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Citations (84)
This report describes parallel studies examining T cell and cytokine responses to Schistosoma mansoni in mice and man. The prevalence of IFNg production amongst murine (C57BL/6) T cell lines and clones, plus good DTH reactivity by IFNg-secreting clones, highlights the predominance of the Th1 response in the pulmonary immunity characteristics of the murine irradiated vaccine model. In human studies, effects of anti-cytokine antibodies on the proliferation of PBMC from human patients to various soluble schistosome antigen preparations have been examined. Data suggest that both Th1 (against early antigens) and Th2 (against late antigens) responses are present. A role for IL-10 is highlighted in chronic intestinal, but not acute or chronic hepatosplenic patients, as a downregulator of responses which are associated with morbidity and are against late stage antigens.
Cellular immunity
Schistosoma
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In the present review, some aspects of the cellular response following the murine Schistosoma mansoni infection are described. Due to the peculiar route used by the schistosome to infect its definitive host, the skin appears as a critical site in which the initial events of the host/parasite relationship occur and where the immune response is initiated. Moreover, the induction and the modulation of the granuloma formation, which represent the main aspect of the pathology of this parasitic disease, is under the control of several cellular populations in which CD4 and CD8 T cells play a key role. The cytokines produced in response to the parasite, such as IL7 in the skin and IFN γ in the liver, seem to influence the further development of immunity against Schistosoma mansoni.
Cellular immunity
Schistosoma
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We have made a comparative analysis of human cellular and antibody responses to membrane associated adult worm antigens (Mb‐A), soluble adult worm antigens (SWAP) and soluble egg antigens (SEA) derived from Schistosoma mansoni . Chronically infected patients with the intestinal (I) and hepatosplenic (HS) forms of the disease as well as non‐infected putative immune ‘endemic normals’ (EN), were studied. We observed that the cellular responses, of individuals, to the two adult worm preparations, SWAP and Mb‐A, may be distinct and can be related to the occurrence of resistance or pathology. The resistant group (EN) presented higher levels of both cellular proliferation, and IFN‐γ production, in response to Mb‐A as compared with SWAP whereas HS individuals presented higher levels of cellular proliferation to SWAP as compared with Mb‐A. Individuals with intestinal disease had similar levels of proliferation to both antigens. The response to SEA by all groups was generally similar, and not predictive of any clinical form. The specific antibody response to the three antigens were in general higher among infected patients than in resistant EN individuals. These results support the hypothesis that the response to adult worm antigens may be pivotal in determining both the development of resistance and severity of disease.
Cellular immunity
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Citations (18)