Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.22.32 (bromelain)
 1,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Highly purified vesicular stomatitis virus (VSV) was obtained from VSV-infected SV40-transformed hamster cell lines. Immunization with this virus protected hamsters against challenge with SV40-transformed cells (TSV5-cl2). This protection was obtained regardless of the source of the SV40-transformed cells (e.g. cat, rat, hamster) used to produce VSV, and was therefore associated with the SV40 tumor-specific transplantation antigen (SV40-TSTA). Furthermore, when grown on spontaneously transformed cell lines or on cells transformed by a different oncogenic DNA virus, such as polyoma virus, the VSV failed to protect against the SV40-induced tumor. It was concluded that the SV40-TSTA activity of purified VSV is due to the incorporation of SV40-TSTA within the viral envelope. When VSV was treated with proteolytic enzymes (bromelain, trypsin) no loss of TSTA-induced tumor rejection was observed, although VSV had lost its ability to induce virus-neutralizing antibody. This clearly demonstrates that the TSTA activity is not related to the viral spikes. Phospholipase C suppressed the TSTA activity but neutralizing activity was still detectable in the anti-VSV sera. The results presented here demonstrate that the protection afforded by VSV is highly specific. It is particularly interesting that SV40-TSTA activity may be conveyed by the lipid core of the viral envelope.
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PMID:SV40 tumor rejection induced by vesicular stomatitis virus bearing SV40 tumor-specific transplantation antigen (SV40-TSTA). I. Specificity of immunoprotection and effect of enzyme treatment on TSTA activity. 7 Dec 74

There is an induction of anti-DNA antibodies in mice following the administration of bacterial lipopolysaccharides, Dextran sulfate and PPD, which is closely associated with the property of these substances to trigger a polyclonal B cell activation. In the experiments model of African trypanosomiasis there is also an intense polyclonal antibody synthesis paralleled by the formation of several autoantibodies: anti-DNA, anti-bromelain treated mouse red blood cells and antithymocyte antibodies.
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PMID:Relevance of polyclonal antibody formation to the development of autoimmunity : the model of African trypanosomiasis. 38 Mar 4

During the propagation of A (H3N2) influenza virus in chick embryos, incorporation of 3H-thymidine into virions takes place, whereas no such incorporation occurs with Newcastle disease virus. Incorporation of 3H-thymidine is a result of DNA synthesis. This virion-associated DNA is present in cores obtained after treatment of virions with bromelain.
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PMID:DNA sequences in influenza virions. 56 83

With age, NZB mice develop anti-RBC autoantibodies resulting in the development of autoimmune hemolytic anemia. We now have evidence that this spontaneous autoantibody response consists of antibodies that are similar in specificity and Id expression to a pathogenic autoantibody (G8) that was cloned from an autoimmune NZB mouse. Similar to autoantibodies eluted from Coombs'-positive mouse E (MRBC), the G8 mAb recognizes native (unmodified) MRBC but not RBC from other species. Interestingly, G8 and four additional mAb bind with a higher titer to bromelain-treated MRBC than to native MRBC. Nucleotide sequence analysis reveals, however, that unlike "natural" antibodies that react solely with bromelain-MRBC, G8 is encoded by a J558 VH gene and a V kappa 12,13 L-chain gene. Thus G8 is clearly distinct from antibodies to bromelain-MRBC which are encoded by unrelated V genes. Instead, the sequence of the G8 VH chain was found to be nearly identical to that of an anti-DNA mAb derived from an MRL-lpr/lpr mouse. The results suggest Coombs'-positive autoantibodies from NZB mice are not derived from "natural" antibodies, but rather, consist of a restricted set of autoantibodies expressing the G8 IdX.
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PMID:A pathogenic monoclonal antibody, G8, is characteristic of antierythrocyte autoantibodies from Coombs'-positive NZB mice. 154 19

Purified populations of B cells expressing the Ly-1 and/or Mac-1 surface Ag were isolated from normal unmanipulated mice by cell sorting. The number of lymphocytes in each population secreting antibodies reactive with DNA, bromelain-treated mouse RBC, phosphorylcholine and TNP-keyhole limpet hemocyanin was quantitated by ELISA spot assay. The proportion of B cells secreting Ig in vivo and the repertoire of antibodies they produced varied as a function of B cell phenotype and location. Among peritoneal lymphocytes, those that were Ly-1+ or Ly-1- Mac-1+ secreted Ig 10 times more frequently that Mac-1- Ly-1- B cells from the same location. In addition, the former populations expressed repertoires that were significantly skewed toward the production of antibodies reactive with bromelain-treated mouse RBC (p less than 0.001). In contrast, splenic B cells expressing the Ly-1 surface Ag did not differ significantly from splenic Ly-1- B cells in their expressed repertoire or frequency of Ig production. B cells isolated from the spleen and peritoneum tended to differ in antibody specificity from bone marrow and lymph node-derived lymphocytes. For example, B cells from the spleen secreted anti-DNA antibodies two to four times more frequently than B cells from other organs. These results demonstrate that phenotype and microenvironment influence the repertoire of antibodies expressed by B cells in vivo.
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PMID:Differences in the repertoire expressed by peritoneal and splenic Ly-1 (CD5)+ B cells. 169 35

Flow cytometry-purified, peritoneal and splenic CD5+ and CD5- B cells from neonatal and adult C57BL/6 mice were studied for expression of VH and Vx gene families in RNA colony blot assays, and for frequencies of clones secreting antibodies to bromelain-treated mouse red blood cells (BrMRBC), single-stranded DNA, trimethyl ammonium and bovine gamma-globulin, by limiting dilution. The results show few overall differences between the two B cell subsets, which both manifest ontogenic D-proximal VH preferences that are lost with age. Biased VH11 expression in CD5 B cells is high in adult peritoneum and spleen but absent in newborns. It only partly correlates with the selection of anti-BrMRBC reactivity, which is considerably higher in peritoneum than in spleen. No particular Vx bias was observed in any of the populations studied with the possible exception of Vx22 in peritoneal CD5+ B cells. We conclude that the antibody repertoire expressed by peritoneal CD5+ B cells of adult mice is not the result of a genetic program, but rather the consequence of local, age-dependent cellular selection mechanisms.
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PMID:Biased VH gene expression in murine CD5 B cells results from age-dependent cellular selection. 171 9

The repertoire of autoantibody-producing B cells was evaluated in a collection of spleen- and thymus-derived hybridomas from 6- and 28-day-old BALB/c mice, which were untreated or prenatally tolerized with trinitrobenzenesulphonic acid (TNBS). MoAb were tested for their reactivity with TNP-BSA and the autoantigens thyroglobulin (TG), myoglobin (MG), actin (AC), cytochrome C (CY), collagen (CO), transferrin (TF), single-stranded DNA (ssDNA), double-stranded DNA (dsDNA), and bromelain-treated mouse red blood cells (BrMRBC). More than 10% of spleen cell (SC)-derived MoAb from 6- and 28-day-old control mice did bind to AC, ssDNA, dsDNA, MY, and TG, the frequency of MoAb reacting with MY, TG, and BrMRBC increasing with age. Thymus cell (TC)-derived hybridomas contained autoreactive clones too, but only few of them produced multireactive MoAb. MoAb from prenatally TNBS-treated mice were more frequently autoreactive than MoAb from control mice, especially if derived from TC hybridomas. The most remarkable difference in the reactivity pattern as compared with MoAb from untreated mice consisted of a significant increase in the frequency of TG-, My-, ssDNA- and above all dsDNA-reactive MoAb, all TC-derived multireactive MoAb binding to dsDNA. The differences in autoreactivity between MoAb from prenatally untreated and TNBS-treated mice as well as age- and organ-related variations support the interpretation that part of the repertoire of naturally activated B cells is not random but is influenced by and responding to the available panel of self antigens.
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PMID:Autoreactive antibodies in thymus and spleen of neonatal and young adult BALB/c mice: influence of prenatal tolerization. 184 57

Autoimmune MRL-lpr/lpr and NZB/W mice spontaneously secrete large quantities of pathogenic IgG1 and IgG2a autoantibodies. NZB mice also produce autoantibodies but these tend to be of the IgM H chain class. This work examines whether differences in the isotype of autoantibody produced by lupus-prone mice reflects differences in the sensitivity of autoreactive B cells to lymphokine-mediated IgG secretion. Twenty-five percent of normal BALB/c B cells produced IgG1 when stimulated in vitro with IL-4 plus LPS. This was comparable with the effect of IL-4 on small resting B cells from MRL-lpr/lpr and NZB/W mice. In contrast, less than 8% of the resting B cells from NZB mice produced IgG1 under these conditions. LPS plus IFN-gamma induced 5% of BALB/c and NZB/W but only 1% of NZB B cells to secrete IgG2a. Because lymphocytes from both young and old NZB mice showed diminished IgG1 and IgG2a secretion after lymphokine treatment, B cells from this strain appeared to be intrinsically resistant to the effects of IL-4 and IFN-gamma. In contrast, a disproportionately large proportion (22%) of B cells from adult MRL-lpr/lpr mice produced IgG2a when treated with IFN-gamma in vitro. Only B cells from MRL-lpr/lpr mice with active disease responded with such high levels of IgG2a production: cells from animals that had not yet developed clinical disease produced normal levels of IgG2a. Within each strain, B cells producing antibodies against autoantigens such as DNA, bromelain-treated mouse RBC and Sm responded to treatment with IL-4 and IFN-gamma in a manner indistinguishable from B cells producing antibodies against conventional Ag such as TNP and ARS.
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PMID:IgG1 and IgG2a production by autoimmune B cells treated in vitro with IL-4 and IFN-gamma. 210 5

Six different endotoxin preparations derived from Escherichia coli and Salmonella typhimurium subspecies were compared as to their potencies to provoke auto-immune phenomena in mice. The numbers of spleen cells forming antibodies to bromelain-treated isologous erythrocytes or anti-DNA antibodies, the serum levels of these auto-antibodies, and the circulating immune complex titres were determined. As far as comparison on a weight base was concerned, S. typhimurium Re-mutant lipopolysaccharide appeared to be the most active preparation in inducing auto-antibody formation. Upon comparison of amounts with equal activity in the limulus amoebocyte lysate assay, however, S. typhimurium lipid A turned out to be the most potent. The contribution of O-type specific polysaccharides, phosphate groups, and the lipid A moiety to the potencies of the endotoxin preparations is discussed.
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PMID:Endotoxin-induced auto-immunity in mice. III. Comparison of different endotoxin preparations. 224 26

New Zealand Black (NZB) mice spontaneously develop an autoimmune hemolytic anemia together with a markedly increased production of polyclonal antibodies. The spontaneous generation of anti-mouse red blood cells (MRBC), anti-bromelain-treated MRBC (BrMRBC) and anti-DNA autoantibodies was compared to the polyclonal antibody formation in irradiated (800 rad) 2-month-old NZB mice reconstituted with bone marrow cells (BMC) from 2- or 10-month-old NZB mice. The injection of 10-month-old NZB BMC markedly accelerated the mortality rate in parallel with the progressive increase of anti-MRBC and anti-BrMRBC autoantibody production, but the spontaneous production of polyclonal IgM antibodies and anti-DNA autoantibodies was completely abolished down to the levels of non-autoimmune mice. In contrast, mice reconstituted with 2-month-old NZB BMC exhibited neither the acceleration of anemia nor the lack of polyclonal antibody production. These results strongly suggest that the spontaneous production of anti-MRBC autoantibodies, including anti-BrMRBC autoantibodies, in the NZB mouse occurs independently of the polyclonal B cell activation, and that they result from a specific immune stimulation, while the anti-DNA autoantibody production is a consequence of polyclonal antibody formation.
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PMID:Spontaneous production of anti-mouse red blood cell autoantibodies is independent of the polyclonal activation in NZB mice. 225 80


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