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E Yefenof

Publications and source records attributed to E Yefenof.

101 records · Page 6Linked to original sources
PubMed1976

Surface markers on human B and T-lymphocytes. IX. Two-color immunofluorescence studies on the association between ebv receptors and complement receptors on the surface of lymphoid cell lines.

Receptors for the third component of complement (C3) were demonstrated on the surface of established human lymphoid cell lines by a membrane fluorescence test with FITC- or TRITC-conjugated antibodies against human C3. Two-color fluorescence staining of EBV receptors and C3 receptors showed complete overlapping of green and red fluorescence. Capping of the EBV receptor induced co-capping of the C3 receptor and vice versa. There was neither overlapping nor co-capping when EBV or C3 receptors were examined in relation to Fc receptors, surface IgM or beta2 microglobulin. The kinetic pattern of EBV receptor capping was identical with the pattern of C3 receptor capping but differed from the pattern of IgM capping. These results suggest a close association between EBV and C3 receptors on the human B-lymphocyte.

B-Lymphocytes↗
PubMed1976

Interaction of antibody and cell surface localized antigen.

The changes occurring in the expression of a membrane-associated antigen following binding of specific antibodies and the fate of the bound antibodies were investigated. Daudi cells, carrying membrane 7S IgM molecules, were coated with radio-labelled anti-IgM antibodies and incubated under culture conditions at 37degrees C. Within 10 h, more than 80% of the cellbound radioactivity was shed from the cells into the culture medium. Concomitantly, IgM molecules were lost, as the cells had a diminished ability to bind a new aliquot of antibody. This phenomenon occurred also when the antibody was used at a low concentration, i.e. did not saturate the cell-surface antigens. The precipitability of the antibody released from the cells with 10% TCA and 40% saturated ammonium sulphate was lower than that of native antibody, indicating some degradation. Also, shed antibody could rebind to fresh Daudi cells less efficiently than native antibody. The presence of immune complexes in the culture supernatants was indicated by the following results: (1) some of the shed radioactivity could bind to IgM-negative but Fc receptor-bearing cells; and (2) immune precipitates of sheep anti-IgM shed from 3H-leucine labelled Daudi cells and of rabbit anti-sheep IgG antibodies contained 3H activity.

Antigen-Antibody Reactions↗
PubMed1976

Surface markers on human B and T lymphocytes. VIII. Association between complement and Epstein-Barr virus receptors on human lymphoid cells.

An association has been found between the Epstein-Barr virus (EBV) and complement (C3d) receptors on human lymphoid cells. The evidence was four-fold: there was a correlation between the expression of these two receptors; inhibition experiments showed that the binding sites probably are close to each other in the cell membrane, although not identical; EBV and complement receptors have been found to co-cap in either order; and lymphoid cell lines lacking complement receptors could not be superinfected with EBV.

Antigens, Viral↗
PubMed1975

Surface markers on human B and T lymphocytes. VII. Rosette formation between peripheral T lymphocytes and lymphoblastoid B-cell lines.

Almost 100% of peripheral T lymphocytes are shown to have the capacity to form rosettes with human lymphoblastoid B-cell lines, predominantly at 4 degrees C and with lines having surface-bound IgG. Blast-transformed T cells retained this capacity and formed rosettes even at 37 degrees C. Unstimulated T cells bound less readily to B-cell blasts, stimulated by pokeweed mitogen for 72 hr. Even though rosettes, formed at 4 degrees C, were stable for several hours at 37 degrees C, no T-cell-mediated cytotoxicity could be detected during overnight incubation. Extreme pH values and trypsinization decreased rosette formation, whereas neuraminidase treatment enhanced the reaction. Rosette formation was independent of bivalent cations and unimpaired in the presence of inhibitors (NaF, NaN3), undiluted human or fetal calf sera, protein A, sonicated sheep erythrocyte membranes, and normal or heat-aggregated human IgG. Anti-Ig, anti-beta2-microglobulin, or anti-T cell sera did not influence rosette formation.

Animals↗
PubMedDate not supplied

CD44 co-stimulates apoptosis in thymic lymphomas and T cell hybridomas.

Thymic lymphomas and hybridomas vary in their sensitivity to dexamethasone (DEX). Identical variance has been demonstrated in our laboratory for apoptosis of such cells by primary thymic epithelial cells or a cell line (TEC). We have also shown that apoptosis induced by TEC was partially mediated by TEC-derived glucocorticoids (GC). We studied the responses of various thymic lymphomas and hybridomas to TEC and DEX. Of these cells, PD1.6 and 2B4 were sensitive whereas B10 were relatively resistant to either inducer. In the present study we found that TEC and DEX synergize in inducing B10 cell apoptosis. B10 cells could also undergo apoptosis by TEC, conditional upon the presence of a TEC-sensitive cell (PD1.6 or 2B4). Contact between TEC and B10 was essential for apoptosis to occur. Thus, TEC may provide two signals, one mediated by GC and the other requiring cell to cell contact. We then analyzed the involvement of co-stimulatory or adhesion molecules in the TEC-induced apoptosis of thymic lymphoma cells. Soluble anti-CD44 antibodies but not anti-CD18, CD2 or CD28, inhibited TEC-induced apoptosis of PD1.6. Dimerization of CD44 by immobilized antibodies augmented DEX-induced apoptosis of all the lymphomas tested. CD44 cross-linkage up-regulated expression of the pro-apoptotic protein Bax, and down-regulated the anti-apoptotic protein, Bclx(L), in the presence of DEX. Taken together, the data suggest that CD44 enhances the apoptotic response of T lymphoma cells to DEX, and that CD44 modulates TEC-induced apoptosis of thymic lymphomas.

Animals↗
PubMedDate not supplied

Interferon amplifies complement activation by Burkitt's lymphoma cells.

Interferon was originally described as an antiviral agent produced shortly after onset of infection with most viruses. However, in addition to inducing an antiviral state, interferon inhibits cell division, increases the expression of cell-surface antigens, boosts the cytotoxic activity of natural killer (NK) cells and modulates several immune functions of lymphocytes and macrophages. Moreover, a special class of interferon (immune interferon or IFN-gamma) is produced by T cells following stimulation with antigen or interaction with mitogens. The different methods by which interferon is induced and its multiple effects suggest that it may be part of a first-line defence system controlling the spread of virus infections and the proliferation of modified 'self' cells that have been affected by virus infection or neoplastic transformation. The ability of certain human lymphoma cells to activate the alternative pathway of complement is well established. Here we show that monoclonal antibody-purified interferon can amplify the ability of certain tumour cells to activate complement via the alternative pathway. This demonstration may reflect an additional, as yet unknown, role of interferon in inducing non-specific anti-tumour immunity.

Burkitt Lymphoma↗