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)

SJL mice are shown to be defective in their ability to develop suppressor cells following stimulation with Con A, a polyclonal T-cell activator. They make a normal proliferative response to this mitogen. In addition to this suppressor T-cell defect, the SJL mouse (unlike most mouse strains) does not develop a spontaneous antibody response to bromelain-treated autologous red blood cells (BrMRBC) in vitro. Although the SJL makes a normal proliferative response to LPS, antibody-forming cells against bromelain-treated autologous red blood cells are not increased following LPS in vivo nor does it manifest an increased response to SRBC or TNP. This may signify the presence of a functional B-cell defect in these animals. DBA mice are also shown, in this report, to have small numbers of antibody-forming cells to bromelain-treated autologous red blood cells but to be capable of responding to LPS in vivo with an increase in SRBC and TNP antibody responses.
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PMID:Immunological defects in SJL mice. 294 46

Spleen and peritoneal cells from unimmunized BALB/c mice were cultured in the presence of LPS for 24 hr and fused to produce hybridomas secreting antibodies against bromelain-treated mouse erythrocytes (BrMRBC). Three clones from spleen cells and eight clones from peritoneal cells were isolated and characterized further. All the monoclonal antibodies had IgMK isotype. Their reactivities against untreated and bromelain-treated erythrocytes from various species were assessed by hemolysis and indirect radioimmunoassay; all the clones had similar antigen specificities. On the isoelectric focussing patterns of light chains, they were separated into two groups, two and nine clones, and all the light chains in each group showed identical patterns. The two groups shared no common idiotope detectable by anti-idiotype antibodies prepared by immunization of rabbits with the monoclonal antibodies, but all the antibodies in each group shared common idiotopes. In each group, one antibody had a unique idiotope different from any other antibody, but eight antibodies in a group shared another identical idiotope. These findings suggest the restricted heterogeneity of anti-BrMRBC antibodies in the mouse.
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PMID:Mouse monoclonal antibodies against bromelain-treated mouse erythrocytes: reactivity with erythrocytes of various species of animals and idiotypes. 310 56

Endotoxin (LPS) and radio-detoxified endotoxin (RD-LPS: 150 kGy 60Co-gamma irradiated) preparations were compared in mice (C57Bl X CBA: F1/Rapo) for capacity to enhance the immune response against sheep red blood cells and to induce the production of antibody against autologous (bromelain-treated) erythrocytes. As RD-LPS retains its capacity to stimulate immune response against heterologous antigen, it may be used as an immuno-adjuvant. The LPS preparation gave rise to a significant increase of autoreactive cells. However, RD-LPS activated the autoantibody forming cells only to a very small degree.
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PMID:Comparison of adjuvanticity and autoantibody inducing capacity of endotoxin and radio-detoxified endotoxin in mice. 330 74

In lymphoid tissues of mice, there exist LPS-reactive B cells which can differentiate to IgM-secreting plaque-forming cells (IgM-PFC) and PFC secreting antibodies against bromelain-treated mouse erythrocytes (BrMRBC) by LPS activation. In this study, four groups of LPS-reactive B cells in spleen, peritoneal cavity and mesenteric lymph nodes from 2- and 10-week-old mice were compared and enumerated as precursors of IgM-PFC and anti-BrMRBC PFC on days 1 and 2 after LPS activation in quantitative culture conditions. The induction of each of four PFC responses in peritoneal cells was sensitive to LPS and anti-mouse IgM antibodies as much as the induction of the respective PFC response in spleen cells. The ratios of four groups of PFC to each other were different among three tissues and between two ages. These findings support the view that the four groups of LPS-reactive B cells in each tissue are mostly in distinct subpopulations of B cells from each other, and the respective groups of different lymphoid tissues at different ages belong to the same subpopulation.
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PMID:Ontogenetic development of lipopolysaccharide-reactive B cells against bromelain-treated mouse erythrocytes in mouse lymphoid tissues. 351 47

Normal mice have large numbers of cells (PFC) making antibody to an autoantigen which is exposed when their own erythrocytes are treated with proteolytic enzymes. Antibody against this antigen can be demonstrated in serum by haemolysis tests against the treated cells; this antibody rises to high levels within 2 to 3 days after injection of E. coli lipopolysaccharide. using quantitative absorption tests we have located the 'bromelain mouse' (BrM) autoantigen in the gastrointestinal tract as well as in erythrocytes; this distribution pattern resembles that of classical blood group antigens. We have described the ontogenetic development of PFC, B cells capable of activation by LPS, serum antibody and antigen. Free antigen is found in the gut shortly after birth. B cells rise rapidly to high levels in the peritoneal cavity, but require a short period of culture to release detectable antibody. PFC and B cells increase more slowly in spleen to adult levels by 3 weeks of age. The serum antibody lags behind PFC development. The pattern is consistent with an early stimulation of B cells in the peritoneal cavity by gut-derived antigen. We discuss the possible relationship of this autoimmune response to high natural responses against other autoantigens in mice, man and other species.
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PMID:Ontogeny of the autoimmune reaction in normal mice to antigens in erythrocytes and gut. 702 Oct 25

Murine peritoneal CD5 B cells include many B cells reactive with bromelain-treated mouse RBC (BrMRBC). Anti-BrMRBC B cells are through to expand after selection by self-antigens, but little is known about signals through their membrane Ig (mIg). Most anti-BrMRBC antibodies use VH11 and V kappa 9 genes, and VH11/V kappa 9-type antibodies are detectable specifically with rabbit anti-idiotype antibodies (here referred to as RAIa). Preincubation of peritoneal cells with RAIa at 37 degrees C before LPS stimulation reduced LPS-induced secretion of RAIa-detectable Ig. To render RAIa-reactive B cells hyporesponsive, a continuous reaction of their mIg with RAIa was necessary. Binding of BrMRBC to RAIa-reactive B cells hardly affected their LPS reactivity. It appears that fresh mIg deliver the suppressive signals after reacted with RAIa, and the degree of hyporesponsiveness of a RAIa-reactive B cell depends on the amount of mIg-RAIa complexes. RAIa-suppressed B cells could regenerate mIg in the absence of RAIa and could respond to LPS to enlarge. It is suggested that binding of RAIa to mIg renders RAIa-reactive B cells without proliferation in an anergy state, where synthesis of secretory Ig is rather specifically suppressed.
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PMID:Signals through membrane Ig of peritoneal CD5 B cells to suppress LPS-induced Ig secretion. 752 81

Part of mouse antibodies reactive with bromelain-treated mouse RBC (BrMRBC) use VH12 and VK4 genes, and VH12/VK4-type antibodies are detectable specifically with rabbit anti-idiotype (Id) antibodies (here referred to as RAIb). This study showed that normal rat sera contained RAIb+ IgM at concentrations of 1-6 micrograms/ml. Rat spleens had many anti-BrMRBC B cells, most of which secreted RAIb+ IgM. Hybridomas of spleen cells from LPS-injected rats were screened with RAIb-binding and BrMRBC-hemolytic activity. We found 48 BrMRBC-hemolytic wells, which included all of 39 RAIb(+)-wells. From anti-BrMRBC wells, 7 RAIb+ monoclonal antibodies (mAb) were isolated. All the RAIb+ mAb could react with phospholipid antigens. Rat RAIb+ antibodies, as well as mouse RAIb+ antibodies, can be regarded as antiphospholipid antibodies reactive with BrMRBC. The interspecies expression of RAIb-Id on mouse and rat anti-BrMRBC antibodies indicates that some (antigenic) selective forces may act strongly to conserve the Id (V genes).
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PMID:Rat antibodies bearing idiotypes of mouse antibodies against bromelain-treated mouse RBC. 771 55

The mechanisms of the suppressive activity of spleen cells from mice undergoing a graft-vs-host reaction (GVH) to non-H-2 histocompatibility Ag were investigated. In our model GVH is induced by injecting bone marrow and spleen cells from B10.D2 (H-2d Mlsb) donors into lethally irradiated (DBA/2 x B10.D2)F1 (H-2d/d Mlsa/b) recipients that differ only with regard to non-H-2 Ag. GVH spleen cells inhibit the mitogenic responses to Con A and LPS, as well as the anti-bromelain-treated mouse RBC (Br-MRBC) antibody response. This suppression was nonspecific and non-H-2-restricted and was not modified after treatment with anti-Thy-1 plus C. Conversely it was abrogated after treatment with L-leucyl methyl ester. These features permitted the identification of non-T cell, L-leucyl methyl ester-sensitive, cells involved in this type of suppression. The suppression mediated by GVH spleen cells was linked to the activity of IFN-gamma and transforming growth factor-beta 1 (TGF-beta 1) (TGF-beta 1 was found to be synthesized by GVH spleen T cells). mAb to IFN-gamma abrogated the suppression of the mitogenic response to Con A and the anti-Br-MRBC response and slightly reversed the suppression of the mitogenic response to LPS. Anti-TGF-beta 1 antibody partially abrogated the suppression of the mitogenic response to LPS and totally abrogated that of the anti-Br-MRBC response but left unmodified the suppression of the mitogenic response to Con A. These results are discussed within the framework of the mechanisms underlying the immunosuppression associated with GVH.
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PMID:Involvement of IFN-gamma and transforming growth factor-beta in graft-vs-host reaction-associated immunosuppression. 845 Feb 27

Spleen, lymph node, and peripheral blood lymphocytes from healthy guinea pigs (gp) were examined for their ability to produce polyreactive autoantibodies to a battery of self-antigens and to cryptic determinants (phosphatidylcholine) on bromelain-treated mouse red blood cells (Br-MRBC). The mouse monoclonal antibody (Mab) 8BE6 anti-gp pan-T (CD5) marker was used for identification of CD5+ B1 cells by the plaque-forming assay (PFC), immunofluorescence, complement-mediated cytotoxicity, and immunocytochemistry. The detection of CD5+ cells by the 8BE6 Mab depended on the method used. They were better demonstrated by cytolysis and immunocytochemistry than by FACS analysis. By the latter method, the level of the CD5+ B cell subpopulation was associated neither with the age of the gp nor with the organ examined. Similarly wide ranges of PFC were detected in untreated or LPS-treated animals regardless of age and organ. The vast majority of the LPS-stimulated IgM antibody-secreting B lymphocytes reacting with the Br-MRBC, and those producing natural autoantibodies, did not bind the 8BE6 Mab.
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PMID:CD5+ and CD5- B1-like lymphocytes in healthy guinea pig. 934 96

Murine B-1 cells are thought to develop from Ig- progenitors early in ontogeny and to expand by self-renewal. To examine the early development of Ig+ precursors of B-1 cells for bromelain-treated mouse RBC, the transient presence of RidA, a rat anti-Id mAb for V(H)11/Vkappa9-type anti-bromelain-treated mouse Abs, was produced in neonatal mice. The presence of RidA during days 0 to 10 of age resulted in an 80% reduction in peritoneal RidA-Id+ B cells and B cells secreting RidA-Id+ Ig after LPS stimulation in 8-wk-old mice. This suggests that most Ig+ precursors for adult RidA-Id+ B cells already exist in 10-d-old mice. However, RidA injected into mice on day 10 had to persist for >4 days to result in a significant reduction in adult B cells. Similarly, although RidA injected into adult mice bound immediately to membrane Ig (mIg) of the peritoneal RidA-Id+ B cells, a RidA persistence for >4 days was required to suppress LPS reactivity of peritoneal and splenic B cells. The binding of RidA to mIg preexisting on B cells has no apparent effect on the ability of neonatal B cells to expand clonally or on the ability of adult B cells to secrete RidA-Id+ Ig after LPS stimulation. Both abilities evidently are suppressed by the accumulation of reaction between freshly expressed mIg and RidA.
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PMID:Induction of tolerance in B-1 cells for bromelain-treated mouse red blood cells by a transient presence of anti-idiotype antibodies in neonatal and adult mice. 959 Feb 26


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