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Biomedical subjects

E W Lamon

Publications and source records attributed to E W Lamon.

At least 73 records · Page 4Linked to original sources
PubMed1976

Antibody-dependent, cell-mediated cytotoxicity with autochthonous lymphocytes and sera after infection with Moloney sarcoma virus.

Antibody-dependent, cell-mediated cytotoxicity in the Moloney sarcoma virus (MSV) system was analyzed in terms of the ability of autochthonous antibody to induce or potentiate cytotoxicity by lymphocytes from animals infected with MSV. As previously demonstrated in microcytotoxicity assays, the lymphocytes from regressor animals taken 30 days after virus infection were consistently more cytotoxic than those from tumor-bearing animals 15 days after infection. Antisera from the regressors potentiated the activity of regressor lymphocytes from the same animals. Also, antisera from tumor bearers, 15 days after virus injection, induced cytotoxicity by the animals' autochthonous lymphocytes which, by themselves, were not cytotoxic. In an independent assay for antibody, both groups of sera produced cytotoxicity by control nonimmune lymphocytes. Specificity controls indicated that both antibody and lymphocytes were required for the induction of cytotoxicity against the target cells in vitro. Normal sera placed on the target cells in the same concentrations induced no cytotoxicity by the immune lymphocytes, and immune sera alone placed on the target cells caused no cytotoxicity. The cooperative activity between antibody and lymphocytes may be a factor that accounts for the observed high incidence of spontaneous tumor regression.

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PubMed1976

IgM complex receptors on subpopulations of murine lymphocytes.

Murine lymphocytes from spleen, lymph node, and thymus were examined for IgM complex receptors. Lymphocytes from all three organs were found to bind SRBC sensitized with IgM from various sources including: primary anti-SRBC serum, murine and rabbit anti-Escherichia coli LPS sera, and a murine IgM myeloma (MOPC 104E). Rosette formation by lymphocytes with IgM-sensitized SRBC was inhibited by soluble antigen-IgM complexes but not by IgM or antigen alone. Rosette formation was also inhibited by human IgM (Fc)5mu but not by Fab mu. Antiserum and complement treatment of the cells and subsequent recovery of the viable cells by trypsinization, filtration, and washing revealed the IgM rosette-forming cell (RFC) in the thymus to be a T cell. Spleen on the other hand was found to contain both B and T cells capable of binding IgM sensitized SRBC. Removal of both B and T cells from spleen cell suspensions eliminated all IgM RFC. The IgM complex receptor was found to be trypsin insensitive. Anti-Ig column fractionation enriched IgM RFC in spleen and lymph node suspensions passed through the columns, whereas cells bearing surface Ig, IgG complex receptors, and C3 receptors were retained in the columns.

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PubMed1975

IgM antibody-dependent cell-mediated cytotoxicity in the Moloney sarcoma virus system: the involvement of T and B lymphocytes as effector cells.

Antibody-dependent cell-mediated cytotoxicity in the Moloney sarcoma virus (MSV) system was analyzed with respect to the subpopulations of effector cells involved in tumor target cell destruction when IgM was used as the sensitizing antibody. With unfractionated sera from animals that had undergone regression primary MSV tumors it was found that macrophages did not contribute to the cytotoxicity induced by normal spleen cells that were syngeneic to the target cells. The IgM fraction of MSV regressor sera was found to induce cytotoxicity against the target cells by immunoadsorbent column-fractionated normal spleen cells, which were either depleted of T cells or B cells, according to the specificity of the columns. Immune IgM was also found to potentiate the activity of MSV regressor spleen cells that had been similarly fractionated. Furthermore, IgM antibody was found to induced cytotoxicity by normal spleen cells which had been depleted of either T or B cells by the appropriate antiserum (anti-T or anti-Ig) in the presence of complement and subsequent recovery of the viable cells by trysinization, filtration, and washing. However, spleen cells treated with both anti-T and anti-Ig sera simultaneously in the presence of complement and subsequet recovery of viable cells, were not induced to be cytotoxic against the IgM-coated tumor target cells. Further support oy T cells was provided by an experiment showing the induction with IgM of cytotoxicity against the target cells by normal thymocytes.

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PubMed1975

Comparison of the allospecific and viral-specific immune responses to irradiated versus formaldehyde-fixed allogeneic Moloney lymphoma cells in CBA mice.

Two groups of adult CBA mice were immunized with 10-7 allogeneic Moloney lymphoma (YAC) cells. These YAC (H-2a) cells, which were either irradiated with 6000 R (Group i) or were formaldehyde fixed (Group II), were injected i.p. at weekly intervals for 3 weeks. Four days following the last injection, sera and lymphocytes were collected and tested in vitro for activity against either allospecific antigens (H-2d target cells) or viral-specific antigens, namely, Moloney leukemia virus (MLV). Both groups of animals developed measurable cellular and humoral immunity to the virally determined antigens. However, only the animals in Group i, immunized with irradiated cells, developed detectable immunity to H-2d. Immune and control lymphocytes were tested in microcytotoxicity tests and by 51Cr release. Antibody was assessed by complement-dependent cytotoxicity, indirect membrane immunofluorescence, virus neutralization, and antibody-dependent lymphocyte cytotoxicity. Group I serum, which had both anti-MLV and anti-H-2 antibodies, was absorbed with either living or formaldehyde-fixed YAC cells. The living cells were able to remove both H-2 and MLV antibodies. On the other hand, the formaldehyde-fixed cells removed no H-2 antibody but were able to remove MLV antibody, although less efficiently than living cells. These data indicate that formaldehyde fixation selectively impaired the H-2 antigens, leaving the viral antigenicity relatively intact. Differences between the immune responses to MLV-determined antigens and to H-2 antigens were demonstrated in many of the parallel in vitro tests.

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PubMed1975

Antibody-dependent lymphocyte cytotoxicity in the murine sarcoma virus system: activity of IgM and IgG with specificity for MLV determined antigen(s).

Antisera with specificity for Moloney leukemia virus-(MLV) determined antigen(s) were studied for their ability to induce MLV antigen bearing target cell reduction by lymphocytes in microcytotoxicity assays. Sera from animals which had regressed Moloney sarcoma virus (MSV) tumors as well as sera from animals with progressively growing MSV tumors were found to induce normal lymphocytes to be active against the targets. Regressor serum was found also to induce cytotoxicity by immune lymphocytes from a tumor-bearing animal 15 days after MSV and from a regressor 50 days after MSV infection. Both the 19S and 7S Sephadex G-200 fractions of the antisera were found to induce cytotoxicity by normal lymphocytes and to potentiate the cytotoxicity of MSV immune lymphocytes. These activities were shown to be IgM and IgG, respectively, by the use of Sepharose-coupled anti-mouse IgM and anti-mouse IgG columns. All activity was removed by passing sera over both columns.

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PubMed1973

The lymphocyte response to primary Moloney sarcoma virus tumors in BALB-c mice. Definition of the active subpopulations at different times after infection.

Adult BALB/c mice were injected with Moloney sarcoma virus (MSV) after which the animals' lymphocytes were examined for activity against Moloney leukemia virus (MLV) antigen-bearing target cells at 5-day intervals for 30 days. Lymphocytes from these animals and appropriately matched controls were fractionated into B cell-deficient (primarily T cells) and T cell-deficient (primarily B cells) subpopulations. Macrophages were removed using iron powder and magnetism. The unfractionated lymphocytes, T cells, and non-T cells were then tested in microcytotoxicity tests. Antigen-specific activity was found in the unfractionated lymphocytes from animals that had not yet developed palpable tumors and from regressor animals. The T cells were active just before tumor development and just after regression; however, by day 30 after virus infection (8-10 days after regression) the T cell subpopulation was much less active. The non-T cell subpopulation was also active before tumor development and soon after regression. However, this activity continued to rise after regression and was highest at 30 days. At day 15 (peak tumor size) neither subpopulation was active. The activity was demonstrated to be specific for the MLV-determined cell surface antigen by testing on control target cells that were MLV antigen negative and by comparison of the inhibitory effects with lymphocytes immune to a nonpertinent antigen as well as normal lymphocytes. The non-T cells were tested for activity before and after removal of macrophages with iron powder and magnetism. Such cells were significantly more active after removal of the macrophages. These data demonstrate specific T cell and non-T cell activity in microcytotoxicity tests with a tumor-specific system and strongly suggest that the non-T cell activity described herein is a B cell function.

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