Publications by authors named "Joskowicz M"

To investigate the development of glomerulopathy during the chronic phase of experimental Chagas' disease, C3H-Hej mice were infected with Trypanosoma cruzi trypomastigotes. Deposits of IgG, IgM, and C3 in renal mesangium were observed by immunofluorescence (IF) to increase in size as a function of time after infection (4-6 months). T.

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Acute Trypanosoma cruzi infection of mice results in a very marked polyclonal activation of B and T lymphocytes, accompanied by high numbers of Ig-secreting PFC and lectin-dependent effector CTL. Treatment of mice with monoclonal anti-L3T4 antibodies from the time of infection (days 0, 4, and 8) completely suppresses the polyclonal PFC response and CTL generation. Treatment of nude mice with antibody does not alter the lipopolysaccharide-induced polyclonal PFC response, and it only modulates the isotypic profile of the PFC response to T.

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Intraperitoneal infection of young adult C57BL/6 males with 10(5) blood or cloned culture forms of Trypanosoma cruzi (CL strain) induced the appearance in spleen, blood, and lymph nodes of cytotoxic effector cells detectable in a lectin-dependent 51Cr-release assay. The effector cells were conventional cytotoxic T lymphocytes (CTL), since they were Thy 1+ and Lyt 2+, and the lysis of tumour target cells was strictly dependent on the presence of lectin. CTL activity is already detectable in spleen 2 days after infection, reaches a peak at 2 weeks, and returns to normal levels during the chronic phase (1 month onwards).

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Lymphoid activity was studied in spleen and lymph node cells from Trypanosoma cruzi-infected mice. Blast transformation in each lymphocyte class was assessed by dual parameter analysis for size and surface markers by both FACS and conventional immunofluorescence, while proliferative activity was measured by tritiated thymidine uptake, autoradiography, and analysis of DNA content in single cells. Acute infection results in rapid blast transformation and proliferative activity of all three lymphocyte classes (Ig+, L3T4+, and Lyt 2+).

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The polyclonal B cell responses induced by Trypanosoma cruzi infection last for at least 6 mo after the inoculation of the parasites. In the acute phase of the disease, B cells from spleen and lymph nodes are largely stimulated, whereas a decrease in bone marrow PFC is observed. As the disease progresses, the numbers of Ig-secreting cells in the spleen, lymph nodes, and bone marrow are all enhanced.

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Mice were acutely and chronically infected with Trypanosoma cruzi and then examined histologically for the presence of lesions in the peripheral nervous system. In acutely infected animals, small lymphocytic and macrophagic infiltrates were found in the nerves in association with intracellular parasites. Little or no nerve damage was present at this stage.

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Infection of mice with Trypanosoma cruzi results in a severe immunosuppression, accompanied by the appearance of autoimmune symptoms. We have previously shown that proliferation and interleukin 2 production by concanavalin A-stimulated T cells from infected mice is severely depressed. In this study we show that at least two phenomena are responsible for this depression.

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Normal C3H/HeJ mice, acutely infected with T. cruzi, develop large numbers of splenic Ig-secreting plaque-forming cells (PFC). IgG2a, IgG2b and IgG1 PFC account for over 90% of all PFC, while the numbers of IgG3- and IgA-secreting PFC are lower than in normal animals.

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Acute infection of mice with Trypanosoma cruzi results in severe immunodepression and the appearance of autoimmune symptoms. In vitro, concanavalin A-stimulated T cells from spleens of infected animals could neither produce nor respond to interleukin 2. Interleukin 2 production was not restored by addition of exogenous interleukin 1, and proliferative response to concanavalin A was not restored by exogenous interleukin 2.

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In vitro cooperative responses between hapten-primed anti-Thy-1.2 plus C-treated spleen cells and carrier-primed T cells have different isotypic patterns depending on the source of the T helper cells. T helper cells from primed lymph node induce IgG1, IgG2a, and IgG2b PFC responses, whereas T helper cells from primed spleen induce only an IgG1 type of response.

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The helper activity of GAT (L-glutamic acid 60-L-alanine 30-L-tyrosine 10)-specific T cells from BALB/c mice has been characterized. The isotypic pattern of the PFC response (plaque-forming cell) obtained in vitro is different depending on the origin of the T helper cells. T helper cells from primed spleen induce a very predominant IgG1 PFC response while T helper cells from primed lymph node induce IgG1-IgG2a- and IgG2b-PFC responses.

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The heterogeneity of the anti-GAT [terpolymer poly(Glu60, Ala30, Tyr10)] response of GAT responder mice has been analyzed. Purified anti-GAT antibodies from BALB/c mice belong only to the gamma 1 kappa subclass. The isoelectric focusing pattern obtained indicates that the anti-GAT antibodies are particularly basic and restricted.

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The biochemical characteristics of immunoglobulin binding factor produced by activated cells (ATC) were investigated. For this purpose, supernatants of ATC were purified by affinity chromatography on insolubilized IgG and the eluted material was iodinated (125I), treated with mercaptoethanol; and run on SDS polyacrylamide gels. The radioactivity was found in two peaks corresponding to m.

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