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)

The effect of cyclosporine (CsA) on the CH12 murine B cell lymphoma was investigated to determine whether sensitivity to this agent is retained by malignant B cells. This tumour produces an antibody to bromelain-treated red blood cells and may represent transformation of a B cell with certain activation properties associated with early resting B cells. In in vitro cultures, the growth and proliferation of CH12 were inhibited by CsA in concentrations of 0.1-1.0 microgram/ml; these levels were ineffective against non-lymphoid tumours, although some non-specific cell toxicity was noted at higher levels. IgM antibody production, as measured by enzyme-linked immunosorbent assay (ELISA), was inhibited over the same range. CH12 cells stimulated by lipopolysaccharide, however, were less sensitive to CsA than untreated cells. These studies indicate that malignant B cells may be sensitive to CsA, perhaps reflecting their derivation from a functionally distinct B cell population with enhanced drug sensitivity.
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PMID:Cyclosporine inhibition of a murine B cell lymphoma. 348 33

The spleens of normal B10.H-2aH-4bp/Wts (2a4b) mice contain cells which, in response to mitogen stimulation, secrete hemolytic antibody specific for a determinant present on both sheep and bromelain-treated mouse erythrocytes. These cells were found to be Ly-1 positive. Approximately 50% of these cells bear surface immunoglobulin (sIg) with the same idiotype as the sIg of a 2a4b-derived B-cell lymphoma, CH12. Backcross analysis revealed H-2 control of the frequency of the idiotype-positive B cell. The regulatory gene did not correlate with the Igh-1 allotype, and analysis of 22 inbred mouse strains mapped the gene to the I-E subregion. Surprisingly, only strains homozygous for Ek alpha expressed the idiotype, and expression was a recessive trait. Possible mechanisms for this control of idiotype expression and its relation to lymphomagenesis are discussed.
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PMID:H-2 control of expression of an idiotype shared by normal B cells and a B-cell lymphoma. 392 82

We have previously described a murine B-cell lymphoma, CH12, the cells of which bear surface IgM reactive with sheep erythrocytes (SRbc) and which could differentiate to secrete hemolytic antibody. The question addressed in this paper was whether differentiation of CH12 cells could be influenced by interaction with regulatory T cells and antigen. If so, we wanted to know whether the conditions required differed from those known to govern similar interactions with normal B cells. We had two reasons for wanting to answer these questions. First, we wondered whether CH12 could be used as a clonal population of indicator cells to study the regulation of B cell differentiation and, second, we wanted to know the extent to which these neoplastic cells were still responsive to normal regulatory signals. The first addresses a major difficulty which must be faced in studies of normal B cell differentiation: to what extent is the interpretation limited by heterogeneity of the B cells used? The second relates to the nature of neoplasia and the possibility that neoplastic cells might be rendered harmless by inducing terminal differentiation. CH12 is one of a series of transplantable B cell lymphomas which arose in B10.H-2aH-4b p/Wts (2a4b) mice, following intense immunization with SRbc. It is a monoclonal tumor, all the cells of which bear membrane IgM(kappa) of a single idiotype, reactive with sheep and chicken Rbc and with bromelain-treated autologous mouse Rbc. The cells express KkAkEk and Dd antigens appropriate to the H-2a haplotype. During the latter stages of growth in vivo or in vitro, a small proportion (less than 3%) of the cells differentiate to secrete hemolytic antibody as measured by the Cunningham assay for plaque forming cells (PFC). We cultured CH12 cells for 3 or 4 days, together with antigen and spleen cells from primed animals, and assayed for PFC induction. Differentiation was induced by spleen cells from SRbc primed 2a4b mice in the presence of SRbc or ChRbc but not rabbit or human erythrocytes. Activity was depleted by treatment of the spleen cells with anti-Thy-1 or anti-Lyt-1 but not anti-Lyt-2 plus complement. Helper cells could also be induced by priming 2a4b mice with ChRbc but not rabbit or human Rbc. Neither of these last two would induce differentiation of CH12, even when both homologous antigen and SRbc were present in the cultures.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Induced differentiation of a B cell lymphoma with known antigen specificity. 624 57