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Beatriz Maria Machado De Medeiros - One of the best experts on this subject based on the ideXlab platform.
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production of autoantibodies associated with Polyclonal Activation in yersinia enterocolitica o 8 infected mice
Microbiology and Immunology, 2005Co-Authors: Orivaldo Pereira Ramos, Eloisa E. E. Silva, Deise Pasetto Falcão, Beatriz Maria Machado De MedeirosAbstract:Polyclonal lymphocyte stimulation is one of the immunomodulatory mechanisms induced by arthritogenic pathogens. In this study we examined the Polyclonal Activation potential of a virulent strain of Y. enterocolitica serotype O:8 (WA 2707+) and its plasmidless isogenic pair (WA 2707−). SPF Swiss mice were infected intragastrically and spleen cells were obtained on days 7, 14, 21, 28, 35 and 42 after infection. The number of cells secreting nonspecific immunoglobulins of IgG, IgM and IgA isotypes was determined by the ELISPOT technique. The presence of serum-specific antibodies was investigated by ELISA and the presence of autoantibodies by dot-blot assay. Although the patterns of infection of the two bacterial strains were almost the same, only the animals infected with the virulent strain presented clinical anomalies. Neither arthritic nor inflammatory signs were observed in the joints of the infected animals. The greatest Activation observed was that of the nonspecific IgM-secreting cells, and their peak of secretion occurred between the 28th and the 42nd day after infection, for both strains of Y. enterocolitica O:8. Only the animals infected with the virulent strain (WA 2707+) produced IgG-specific antibodies in the serum, from the 28th day after infection. The serum of animals infected with either strain showed reactivity to all the autologous constituents tested, mainly on the 28th and 42nd day after infection. It was concluded that infection of mice with either the virulent strain of Y. enterocolitica O:8 or with its plasmidless isogenic pair resulted in the Polyclonal Activation of the splenic B lymphocytes including some autoreactive clones.
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yersinia enterocolitica o 3 isolated from patients with or without reactive arthritis induces Polyclonal Activation of b cells and autoantibody production in vivo
Autoimmunity, 2003Co-Authors: Eloisa E. E. Silva, Orivaldo Pereira Ramos, Deise Pasetto Falcão, Tais Maria Bauab, Beatriz Maria Machado De MedeirosAbstract:The mechanisms by which arthritis-provoking pathogens such as Yersinia enterocolitica interact with the human immune system to produce inflammatory synovitis are not well known. One of the immunomodulating mechanisms used against these pathogens is the Polyclonal Activation of lymphocytes. In this study, we investigated the extent of the B-lymphocyte Activation induced in mice by a strain of Y. enterocolitica O:3 (FCF 526) isolated from a patient with arthritis, and compared it with two other strains, a virulent one (FCF 397[+]) isolated from a patient without arthritis and its plasmidless isogenic pair (FCF397[-]). Also we investigated the production of autoantibodies in mice infected with these different strains. SPF Swiss mice were infected intravenously with a suspension of Y. enterocolitica. Spleen cells were taken on days 7, 14, 21 and 28 after infection and the number of cells secreting nonspecific and specific antibodies of IgG1, IgG2a, IgG2b, IgG3, IgM and IgA isotypes were determined by the ELIS...
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Polyclonal Activation as a consequence of infection of mice with Yersinia enterocolitica O:3 isolated from patients with or without arthritis.
Advances in Experimental Medicine and Biology, 2003Co-Authors: Beatriz Maria Machado De Medeiros, Eloisa E. E. Silva, Orivaldo Pereira Ramos, Deise Pasetto FalcãoAbstract:It was observed Polyclonal Activation of B-lymphocytes with all the bacterial strains tested. The IgG2a and IgG3 isotypes were that which present the major Activation. The three bacterial strains stimulated the production of autoantibodies against all the autologous constituents tested.
Adriana Gruppi - One of the best experts on this subject based on the ideXlab platform.
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Polyclonal b cell Activation in infections infectious agents devilry or defense mechanism of the host
Journal of Leukocyte Biology, 2007Co-Authors: Carolina L. Montes, Eva V Acostarodriguez, Maria C Merino, Daniela A Bermejo, Adriana GruppiAbstract:Polyclonal B cell Activation is not a pe- culiar characteristic to a particular infection, as many viruses, bacteria, and parasites induce a strong Polyclonal B cell response resulting in hy- per--globulinemia. Here, we discuss the different roles proposed for Polyclonal B cell Activation, which can be crucial for early host defense against rapidly dividing microorganisms by contributing antibodies specific for a spectrum of conserved structures present in the pathogens. In addition, Polyclonal B cell Activation can be responsible for maintenance of memory B cell responses because of the continuous, unrestricted stimulation of memory B cells whose antibody production may be sustained in the absence of the antigens binding- specific BCR. Conversely, Polyclonal Activation can be triggered by microorganisms to avoid the host- specific, immune response by activating B cell clones, which produce nonmicroorganism-specific antibod- ies. Finally, some reports suggest a deleterious role for Polyclonal Activation, arguing that it could poten- tially turn on anti-self-responses and lead to autoim- mune manifestations during chronic infections. J. Leukoc. Biol. 82: 1027-1032; 2007.
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trypanosoma cruzi mitochondrial malate dehydrogenase triggers Polyclonal b cell Activation
Clinical and Experimental Immunology, 2002Co-Authors: Carolina L. Montes, Elina I Zuniga, Jesus Vazquez, C Arce, Adriana GruppiAbstract:SUMMARY It has been proposed that Trypanosoma cruzi, the aetiologic agent of Chagas’ disease, produces mitogenic substances responsible for the Polyclonal B-cell Activation observed during the acute phase of the infection. Isolation and characterization of the molecules involved in the induction of Polyclonal Activation observed during infectious diseases have posed a great challenge for the immunologist over the last decade. In this work we report that a 33 kD protein obtained from an alkaline fraction of T. cruzi epimastigotes (FI) stimulates proliferation and promotes differentiation into antibody-secreting cells of normal murine B cells in a T-cell independent manner. By flow cytometry we also found that the 33 kDa protein induces an increase in the expression of MHC class II and B7.2 but not B7.1 molecules on the B-cell surface. Sequencing by mass spectrometry identified the T. cruzi 33 kD protein as hypothetical oxidoreductase, a member of the aldo/ketoreductase family. In this report we demonstrate that this protein is also present in the infective bloodstream trypomastigote form of the parasite and was identified as T. cruzi mitochondrial malate dehydrogenase (mMDH) by enzyme activity and by Western blotting using a specific mMDH Polyclonal antiserum. The biologic relevance of mMDH-induced Polyclonal Activation concerning T. cruzi infection is discussed.
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Trypanosoma cruzi Cytosolic Alkaline Antigens (FI) Induce Polyclonal Activation in Murine Normal B Cells
Scandinavian Journal of Immunology, 1996Co-Authors: Carolina L. Montes, E. Vottero‐cima, Adriana GruppiAbstract:: Several reports have described Polyclonal Activation in mice acutely infected with Trypanosoma cruzi. The aim of this work was to analyse the participation of one T. cruzi antigenic fraction in this immunological event. The antigen selected was FI, an antigenic fraction of pI 7-9 obtained from T. cruzi cytosol separated by isoelectricfocusing. FI is constituted by molecules with molecular weights of around 60 and 20 KDa. The authors assayed the ability of this antigenic fraction to induce Polyclonal Activation of spleen mononuclear cells from normal (NSMC) BALB/c mice. NSMC showed a marked lymphoproliferative response measured by 3H-thymidine incorporation after 3 days of culture in presence of FI. The values reached by FI-stimulated cells were 10 times higher than the controls (non-stimulated cells). This effect was dose-dependent. Furthermore, the authors observed that a purified T-cell population in the presence of adherent cells was unaffected by FI. Additionally, in a culture of NSMC, FI stimulated the proliferation of B cells as observed by the increase of the percentage of B220+ cells determined by FACS using FITC-conjugated anti-mouse B220. The authors noticed that the percentage of B220+Ly1+(CD5) populations in the presence of FI did not change with respect to the control (non-stimulated cells), indicating that FI expanded both conventional and CD5+ B cells. The isotypic pattern of the antibodies produced after 6 days of culture of NSMC in the presence of FI was predominantly IgM, which reacted with highly conserved antigens such as actin, myosin, myoglobin, thyroglobulin and carbonic anhydrase, but did not react with FI. A slight increase of IgG1 and IgG3 with respect to the control was observed but no changes on the levels of IgG2 was noticed. These results indicate that FI promotes Activation, proliferation and differentiation in antibody-secreting cells of normal murine B lymphocytes.
Peter G W Plagemann - One of the best experts on this subject based on the ideXlab platform.
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Polyclonal Activation of b cells by lactate dehydrogenase elevating virus is mediated by n glycans on the short ectodomain of the primary envelope glycoprotein
Advances in Experimental Medicine and Biology, 2001Co-Authors: Peter G W Plagemann, Quentin A Jones, William A CafrunyAbstract:The common strains of lactate dehydrogenase-elevating virus (LDV-P and LD-vx) are primary examples for viruses that cause a permanent Polyclonal Activation of B cells that results in IgG2a hyper-gammaglobulinemia and the generation of autoantibodies and circulating immune complexes in their host, the mouse (Notkins et al., 1966; Coutelier and van Snick, 1985; Li et al, 1990). Plasma IgG2a levels increase from generally below 0.5 mg/ml to 2-6 mg/ml by two weeks post infection (p.i.) and remain elevated thereafter (see later). LDV-P/vx cause life-long persistent viremic infections (see Fig. 1A) which are maintained by continuous rounds of replication in a renewable subpopulation of macrophages and resistance to host immune responses (Plagemann, 1996). Previous results have shown that the single neutralization epitope located on the short (about 30 amino acids long) ectodomain of the primary envelope glycoprotein, VP-3P, carries three large N-glycan chains in LDV-P and LDV-vx (see Fig. 1A insert) that suppress the immunogenicity of the epitope and impair antibody neutralization of the virions of these quasispecies (Chen et al, 2000; Plagemann et al., 1999). The present results indicate that the three N-glycans on the VP-3P ectodomains of LDV-P/vx also play a critical role in the Polyclonal Activation of B cells by these LDVs.
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n glycans on the short ectodomain of the primary envelope glycoprotein play a major role in the Polyclonal Activation of b cells by lactate dehydrogenase elevating virus
Journal of General Virology, 2000Co-Authors: Peter G W Plagemann, Quentin A Jones, William A CafrunyAbstract:The common biologically cloned isolates of lactate dehydrogenase-elevating virus (LDV-P and LDV-vx) invariably cause a Polyclonal Activation of B cells in immunocompetent mice. It is recognized by an at least 10-fold increase in plasma IgG2a levels and the de novo formation of immune complexes that most likely consist of autoantibodies and their antigens. The present study indicates that three closely spaced N-glycans on the short ectodomain of the primary envelope glycoprotein, VP-3P, of LDV-P/vx, play a major role in inducing the Polyclonal proliferation of B cells. IFN-γ then seems to mediate the differentiation of the activated B cells to IgG2a-producing plasma cells. These conclusions are based on the finding that the IgG2a hypergammaglobulinaemia and immune complex formation were much lower in mice that were infected with LDV variants (LDV-C and LDV-v) whose VP-3P ectodomains lack two of the three N-glycans than in LDV-P/vx infected mice. In contrast, the VP-3P ectodomains of three neutralization escape variants of LDV-C/v whose VP-3P ectodomains possess three N-glycosylation sites caused a Polyclonal Activation of B cells comparable to that of LDV-P/vx.
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neonatal infection of mice with lactate dehydrogenase elevating virus results in suppression of humoral antiviral immune response but does not alter the course of viraemia or the Polyclonal Activation of b cells and immune complex formation
Journal of General Virology, 1994Co-Authors: Raymond R R Rowland, Chen Even, Grant W Anderson, Zongyu Chen, Bugen Hu, Peter G W PlagemannAbstract:Neonatal infection of FVB mice with lactate dehydrogenase-elevating virus (LDV) prevented the normal formation of anti-LDV antibodies observed in mice infected at 5 days of age or older. Even 22 weeks post-infection, the concentration of circulating anti-LDV antibodies in neonatally infected mice was insignificant. However, the time course and level of persistent viraemia were the same in neonatally infected mice lacking anti-LDV antibodies as in mice infected at 5 or 15 days of age which developed normal antiviral immune responses. The results support the view that LDV replication in mice is unaffected by antiviral immune responses and instead is primarily dependent on the rate of regeneration of LDV-permissive macrophages. This view is further supported by the following findings. Treatment of mice with cyclophosphamide or dexamethasone, which are known to increase plasma LDV levels, increased the proportion of LDV-permissive macrophages in the peritoneum. Injection of mice with interleukin-3, which is known to stimulate macrophage development, increased plasma LDV levels in persistently infected mice 10- to 100-fold. During the first month of age when mice possess a higher proportion of LDV-permissive macrophages than older mice and peritoneal macrophages exhibit self-sustained growth, the persistent plasma LDV titres were also 10- to 100-fold higher than in older mice. The Polyclonal Activation of B cells induced by LDV that results in a permanent elevation of IgG2a or IgG2b in the circulation, and the formation of 180K to 300K immune complexes containing IgG2a or IgG2b were also the same in neonatally infected mice and mice infected 5 or 15 days after birth. Thus, the Polyclonal Activation of B cells occurs in the absence of an antiviral humoral immune response and the immune complexes do not contain anti-LDV antibodies. The immune complexes probably consist of autoantibodies formed in the course of the Polyclonal Activation of B cells and their cellular antigens.
William A Cafruny - One of the best experts on this subject based on the ideXlab platform.
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Polyclonal Activation of b cells by lactate dehydrogenase elevating virus is mediated by n glycans on the short ectodomain of the primary envelope glycoprotein
Advances in Experimental Medicine and Biology, 2001Co-Authors: Peter G W Plagemann, Quentin A Jones, William A CafrunyAbstract:The common strains of lactate dehydrogenase-elevating virus (LDV-P and LD-vx) are primary examples for viruses that cause a permanent Polyclonal Activation of B cells that results in IgG2a hyper-gammaglobulinemia and the generation of autoantibodies and circulating immune complexes in their host, the mouse (Notkins et al., 1966; Coutelier and van Snick, 1985; Li et al, 1990). Plasma IgG2a levels increase from generally below 0.5 mg/ml to 2-6 mg/ml by two weeks post infection (p.i.) and remain elevated thereafter (see later). LDV-P/vx cause life-long persistent viremic infections (see Fig. 1A) which are maintained by continuous rounds of replication in a renewable subpopulation of macrophages and resistance to host immune responses (Plagemann, 1996). Previous results have shown that the single neutralization epitope located on the short (about 30 amino acids long) ectodomain of the primary envelope glycoprotein, VP-3P, carries three large N-glycan chains in LDV-P and LDV-vx (see Fig. 1A insert) that suppress the immunogenicity of the epitope and impair antibody neutralization of the virions of these quasispecies (Chen et al, 2000; Plagemann et al., 1999). The present results indicate that the three N-glycans on the VP-3P ectodomains of LDV-P/vx also play a critical role in the Polyclonal Activation of B cells by these LDVs.
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n glycans on the short ectodomain of the primary envelope glycoprotein play a major role in the Polyclonal Activation of b cells by lactate dehydrogenase elevating virus
Journal of General Virology, 2000Co-Authors: Peter G W Plagemann, Quentin A Jones, William A CafrunyAbstract:The common biologically cloned isolates of lactate dehydrogenase-elevating virus (LDV-P and LDV-vx) invariably cause a Polyclonal Activation of B cells in immunocompetent mice. It is recognized by an at least 10-fold increase in plasma IgG2a levels and the de novo formation of immune complexes that most likely consist of autoantibodies and their antigens. The present study indicates that three closely spaced N-glycans on the short ectodomain of the primary envelope glycoprotein, VP-3P, of LDV-P/vx, play a major role in inducing the Polyclonal proliferation of B cells. IFN-γ then seems to mediate the differentiation of the activated B cells to IgG2a-producing plasma cells. These conclusions are based on the finding that the IgG2a hypergammaglobulinaemia and immune complex formation were much lower in mice that were infected with LDV variants (LDV-C and LDV-v) whose VP-3P ectodomains lack two of the three N-glycans than in LDV-P/vx infected mice. In contrast, the VP-3P ectodomains of three neutralization escape variants of LDV-C/v whose VP-3P ectodomains possess three N-glycosylation sites caused a Polyclonal Activation of B cells comparable to that of LDV-P/vx.
Eloisa E. E. Silva - One of the best experts on this subject based on the ideXlab platform.
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production of autoantibodies associated with Polyclonal Activation in yersinia enterocolitica o 8 infected mice
Microbiology and Immunology, 2005Co-Authors: Orivaldo Pereira Ramos, Eloisa E. E. Silva, Deise Pasetto Falcão, Beatriz Maria Machado De MedeirosAbstract:Polyclonal lymphocyte stimulation is one of the immunomodulatory mechanisms induced by arthritogenic pathogens. In this study we examined the Polyclonal Activation potential of a virulent strain of Y. enterocolitica serotype O:8 (WA 2707+) and its plasmidless isogenic pair (WA 2707−). SPF Swiss mice were infected intragastrically and spleen cells were obtained on days 7, 14, 21, 28, 35 and 42 after infection. The number of cells secreting nonspecific immunoglobulins of IgG, IgM and IgA isotypes was determined by the ELISPOT technique. The presence of serum-specific antibodies was investigated by ELISA and the presence of autoantibodies by dot-blot assay. Although the patterns of infection of the two bacterial strains were almost the same, only the animals infected with the virulent strain presented clinical anomalies. Neither arthritic nor inflammatory signs were observed in the joints of the infected animals. The greatest Activation observed was that of the nonspecific IgM-secreting cells, and their peak of secretion occurred between the 28th and the 42nd day after infection, for both strains of Y. enterocolitica O:8. Only the animals infected with the virulent strain (WA 2707+) produced IgG-specific antibodies in the serum, from the 28th day after infection. The serum of animals infected with either strain showed reactivity to all the autologous constituents tested, mainly on the 28th and 42nd day after infection. It was concluded that infection of mice with either the virulent strain of Y. enterocolitica O:8 or with its plasmidless isogenic pair resulted in the Polyclonal Activation of the splenic B lymphocytes including some autoreactive clones.
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yersinia enterocolitica o 3 isolated from patients with or without reactive arthritis induces Polyclonal Activation of b cells and autoantibody production in vivo
Autoimmunity, 2003Co-Authors: Eloisa E. E. Silva, Orivaldo Pereira Ramos, Deise Pasetto Falcão, Tais Maria Bauab, Beatriz Maria Machado De MedeirosAbstract:The mechanisms by which arthritis-provoking pathogens such as Yersinia enterocolitica interact with the human immune system to produce inflammatory synovitis are not well known. One of the immunomodulating mechanisms used against these pathogens is the Polyclonal Activation of lymphocytes. In this study, we investigated the extent of the B-lymphocyte Activation induced in mice by a strain of Y. enterocolitica O:3 (FCF 526) isolated from a patient with arthritis, and compared it with two other strains, a virulent one (FCF 397[+]) isolated from a patient without arthritis and its plasmidless isogenic pair (FCF397[-]). Also we investigated the production of autoantibodies in mice infected with these different strains. SPF Swiss mice were infected intravenously with a suspension of Y. enterocolitica. Spleen cells were taken on days 7, 14, 21 and 28 after infection and the number of cells secreting nonspecific and specific antibodies of IgG1, IgG2a, IgG2b, IgG3, IgM and IgA isotypes were determined by the ELIS...
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Polyclonal Activation as a consequence of infection of mice with Yersinia enterocolitica O:3 isolated from patients with or without arthritis.
Advances in Experimental Medicine and Biology, 2003Co-Authors: Beatriz Maria Machado De Medeiros, Eloisa E. E. Silva, Orivaldo Pereira Ramos, Deise Pasetto FalcãoAbstract:It was observed Polyclonal Activation of B-lymphocytes with all the bacterial strains tested. The IgG2a and IgG3 isotypes were that which present the major Activation. The three bacterial strains stimulated the production of autoantibodies against all the autologous constituents tested.
