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Biomedical subjects

M Jondal

Publications and source records attributed to M Jondal.

At least 163 records · Page 9Linked to original sources
PubMed1978

Spontaneous and lectin-dependent cellular cytotoxicity by lymphocyte subpopulations against cell lines susceptible or resistant to spontaneous cytotoxicity.

In the present study we have investigated whether cell lines, which are resistant to spontaneous cytotoxicity, can be killed by lectin-dependent cellular cytotoxicity (LDCC), the expression of EAC (7S) receptors on LDCC effector cells, and the relationship between spontaneous cytotoxicity and LDCC when EAC (7S) receptor-positive or -negative subpopulations are tested against different target cell lines. We found that target cells which are resistant to spontaneous cytotoxicity can, indeed, be killed by LDCC, and that there is an inverse relationship between spontaneous cytotoxicity and LDCC, both when unfractionated lymphocytes were tested against different target cells and when fractionated cells were tested against cell lines highly susceptible to spontaneous cytotoxicity. The implications of these findings, in relation to the relative specificity of the spontaneous cytotoxicity system, are discussed.

Cell Line↗
PubMed1977

Spontaneous human lymphocyte-mediated cytotoxicity against tumor target cells. II. Is the complement receptor necessarily present on the killer cells?

The effect of various lymphocyte depletion techniques on SLMC effector cell activity against the cell line K562 could be attributed to the effects that these procedures had on the proportions of Fc/C3 receptor-bearing cells in the preparations. depletion of cytotoxic activity by removal of Fc receptor-bearing cells could be augmented by the presence of complement on the 7S-EA indicator cells used for rosette depletion. Two methods of assessing the presence of surface receptors on cytotoxic cells are presented: (1) linear regression analysis of spontaneous cytotoxicity plotted as a function of the proportions of receptor-bearing cells remaining after various depletion techniques; and (2) the use of a mathmatical formula to estimate the proportion of cytotoxic cells with any particular receptor, based on the effects of receptor-bearing cell depletion. Linear regression analysis of cytotoxicity vs the proportions of SRBC, Fc or C3 receptor-bearing cells demonstrated that all cytotoxic cells had the Fc receptor, but that cytotoxicity could still occur in the absence of cells with the C3 receptor. This indicated that the C3 receptor is not necessary for the demonstration of SLMC activity. The mathematical formula to predict cytotoxicity after depletion of C3 receptor-bearing lymphocytes showed, however, that a significant proportion of the Fc receptor-positive killer cells were also C3 receptor-positive. No direct evidence was found to support a role for T cells in SLMC, although E rosette depletion resulted in lower than expected cytotoxicity in view of the number of Fc receptor-bearing cells remaining in the preparation.

Antibodies, Neoplasm↗
PubMed1977

Somatic cell hybrids between human lymphoma lines. III. Surface markers.

Hybrids between two human lymphoma lines, Raji and Daudi (8A) and Raji BJAB (83) were examined for genetically determined and/or differentiation-related surface markers. HL-A B ce-l alloantigens, Fc and complement receptors, EBV receptors and beta2 microglobulin showed an autonomous ("co-dominant") expression in the hybrid. This is in contrast to most previous studies on other differentiation markers, involving as a rule crosses between cells of different lineages, where the differentiated pattern usually became "eclipsed" in the hybrid. Staining of activated complement and complement consumption tests showed intermediate or partially suppressed expression in the hybrids. This may be viewed in relation to the fact that these reactions do not merely depend on complement binding to the receptor, but also on subsequent activation and binding of the activated complement. A more complex interaction is also suggested for immunoglobulin production. Surface immunoglobulin showed a suppressive or intermediate pattern in both hybrids, whereas intracellular kappa chain production showed an amplification in the 83 hybrid. The beta2 microglobulin deficiency of the Daudi parent was corrected in the Raji/Daudi hybrid. Two new HL-A specificities,A10 and BW17, appeared on this hybrid which were not present on the parental lines. This suggests that the HL-A deficiency of the Daudi cell is due to its lack of beta2 microglobulin.

B-Lymphocytes↗
PubMed1977

Antibody-dependent cellular cytotoxicity (ADCC) against Epstein-Barr virus-determined antigens II. Induction of ADCC by FC-FC receptor bridging.

Four different methods to test antibody-dependent cellular cytotoxicity (ADCC) against Epstein-Barr virus (EBV) determined antigens were analysed. It was found that optimal ADCC was obtained if viral antigens were present during the cytotoxicity reaction and that killing probably was mediated by EBV-related immune-complexes forming Fc-Fc receptor bridges between Fc receptor-bearing effector cells and Fc receptor-bearing target cells. Only lymphoid target cells with a high expression of Fc receptors were found to be susceptible in this particular system.

Animals↗
PubMed1977

Antibody-dependent cellular cytotoxicity (ADCC) against Epstein-Barr virus-determined antigens. III. Reactivity in sera from patients with Burkitt's lymphoma in relation to tumour development.

Sera from patients with Burkitt's lymphoma (BL) were tested for antibody-dependent cellular cytotoxicity (ADCC) against Epstein-Barr virus (EBV) determined antigens and for antibodies directed against various EBV-specific antigens. No correlation was found between EBV serology and ADCC in sera selected for high or low titres against the membrane antigens (MA) or in consecutive sera from three patients with isolated late tumour recurrences. Furthermore, no correlation was found between ADCC and tumour development.

Antigens, Viral↗
PubMed1976

Inducibility of the Epstein-Barr virus (EBV) cycle and surface marker properties of EBV-negative lymphoma lines and their in vitro EBV-converted sublines.

Two EBV-negative lymphoma lines of human B-cell origin, BJAB and Ramos, were compared with altogether six of their in vitro EBV-converted, EBNA- and EBV-DNA-carrying sublines (four of Ramos and two of BJAB derivation). All converted lines closely resembled the parental line with regard to karyotype and HL-A and B antigen typing. Induction of EBV antigens (EA and VCA) by P3HR-1 virus superinfection was either similar in the converted and the negative lines, or somewhat increased in certain converted lines. These findings argue against a simple, virally determined repressor model and emphasize the role or cellular controls in restricting the EBV cycle in virus-carrying B-lymphocyte lines of human origin. IUdR inducibility varied in the different converted lines. There was a possible relationship between average number of EBV-genome equivalents per cell and inducibility. Converted sublines did not differ from the original negative lines with regard to surface immunoglobulin and Fc receptors. There was a dramatic increase in complement-consuming ability, however, following EBV conversion. Among the EBV-positive lines, there was a linear relationship between complement-consuming and EBV-receptor activity, the latter measured by a quantitative absorption test.

Antigens, Viral↗
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

Killer cells: a functional comparison between natural, immune T-cell and antibody-dependent in vitro systems.

Previous reports have shown that spleen cells from nonimmune adult mice of certain strains do regularly kill Moloney leukemia virus-induced lymphomas in short-term 51Cr release assays. This naturally occuring killer (NK) cell had low adherent properties and had the morphological appearance of a lymphocyte. Still it lacked surface characteristics of mature T or B lymphocytes. In the present report a functional study was carried out, comparing in parallel the NK system, the T-cell killing across an H-2 barrier (anti-P815), and the antibody-dependent cell-mediated chicken red blood cell (CRBC) system. In contrast to the effector cells in the CRBC system, the NK cells were insensitive to erythrocyte antibody complement (EAC) rosette depletion and would pass through nylon wool columns. NK activity was not inhibited by the presence of heat-aggregated human or mouse gamma globulin, in contrast to the strong inhibition noted in the CRBC system. Sensitivity to trypsin pretreatment was noted in the NK system as well as in the immune P815 system, whereas the CRBC system was relatively trypsin resistant. Antitheta plus complement eliminated the anti-P815 activity, but did not touch the NK activity. The present results thus further distinguish the NK cell from cytotoxic T lymphocytes or from antibody-dependent killer cells.

Animals↗
PubMed1976

EBV-determined nuclear antigen (EBNA)-positive cells in the peripheral blood of infectious mononucleosis patients.

After removal of SRBC rosette-forming T-cells from the peripheral blood, the residual, largely B-lymphocyte fraction of five infectious mononucleosis patients was found to contain 0.5-2% blast cells, positive for the EBV-determined nuclear antigen (EBNA). There was a rough parallelism between the presence of large lymphoblasts in the hematological smear, EBNS-positive large blasts in the B-cell fraction and the ability of the T-cell fraction to exert an EBV-specific lymphocytotoxicity on established cell lines in vitro. EBNA-positive B-cells and EBV-specific killer T-cells disappeared after the acute phase of the disease.

Acute Disease↗
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↗
PubMed1976

Epstein-Barr virus interactions with human lymphocyte subpopulations: virus adsorption, kinetics of expression of Epstein-Barr virus-associated nuclear antigen, and lymphocyte transformation.

In order to further understand Epstein-Barr virus (EBV)-lymphocyte interactions, we investigated a chain of events including: (i) EBV binding to human lymphocyte subpopulations; (ii) the earliest appearance of EBV-determined nuclear antigen (EBNA) in the lymphocytes after EBV infection; and (iii) establishment of continuous lymphoblastoid cell lines (LCL) by infecting with EBV different types of lymphocyte preparations from the same as well as from different donors. By using direct membrane immunofluorescence assay, we found that only a small fraction of human peripheral blood and cord blood lymphocytes (CBL), and possibly less than 31% of the T cell-depleted lymphocyte population, carry receptors for P3HR-1 strain of EBV. The number of cells carrying receptors for EBV did not vary considerably among different blood lymphocyte populations from several normal donors. EBV adsorption on lymphocyte subpopulations showed that purified thymus-dependent (T) cells and thymocytes did not adsorb EBV, in contrast to T cell-depleted lymphocyte populations and lymphoid cells from fetal liver and spleen. In CBL infected with EBV strain B95-8, EBNA was detected by anti-complement immunofluorescence as early as 18 h after infection. This indicates that EBNA is the earliest detectable EBV-determined intracellular antigen to appear after infection and before or during lymphocyte transformation by EBV. Transformation was observed only in lymphocyte cultures containing detectable thymus-independent B cells but not in cultures of purified T cells. With one exception (es-b-1), all the EBV-transformed LCL from different origins carried surface-bound immunoglobulins (a B cell marker). These included also the 10 LCL obtained by infecting cultures of adherent cells from different donors. With regard to its surface markers, ES-B-1 appeared to be an exceptional EBV genome-carrying line, and it also lacked the ability to form spontaneous rosettes with sheep erythrocytes (a T cell marker). Therefore, it is possible that ES-B-1 was derived from an atypical B cell or B cell precursor or from a so-called "null cell" transformed by EBV.

Adsorption↗