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Results for “Cytotoxicity, Immunologic”

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At least 19 recordsLinked to original sources
PubMed1977

Renal donor pretreatment with cytotoxic agents: immunologically ineffective and damaging to the graft.

Simultaneous double renal allografts were performed in 32 dogs to evaluate the effect of pretreatment of the donor kidney with either Medrol, cytoxan, and methotrexate or medrol and procarbazine. There was no prolongation of survival of treated allografts. Immunosuppressive therapy for the transplanted animal unmasked a pretreatment injury of the pretreated kidney. Treatment of an autograft kidney in an intermediate host produced a cytotoxic tubular lesion in the kidney and also appeared to protect the kidney from the double ischemic insult incurred during the transplantation procedure. Pretreatment of dog donors of renal allografts with cytotoxic agents thereby offers no immunologic advantage for graft survival and produces a cytotoxic tubular lesion that is detrimental to kidney survival when ischemic and immunologic injury is minimal.

Animals↗
PubMed1979

Antibody-induced changes in levels of cyclic adenosine monophosphate in leukaemic lymphocytes.

When L2C leukaemic B lymphocytes from guinea-pigs were incubated in vitro with antibody directed to their surface immunoglobulin (Ig), a rapid rise in intracellular adenosine 3':5'-phosphate (cyclic adenosine monophosphate, cAMP) was observed. Estimation of cAMP was by a protein-binding assay using bovine adrenal protein kinase. Increases up to 30-fold occurred within 30 seconds of incubation at 37 degrees C, to be succeeded by a fall which reached the basal level between 5 and 7 min. The response was proportional to the amount of antibody present. Cross-linking of surface Ig by the antibody was necessary, bivalent (Fab'gamma)2 from the antibody gave a rise in cAMP similar to that given by the parent molecule, whereas monomeric Fab'gamma was ineffective unless it was subsequently cross-linked by anti-antibody. The rise was too rapid to have required capping of the surface Ig for its induction. Not all perturbations of the plasma membrane by antibody induce such a surge in cAMP, since anti-beta2 microglobulin, also reacting with the lymphocyte surface, failed to alter cAMP concentration. The results emphasize that immunotherapy can be influenced by antibody altering the metabolic activity of target cells, quite apart from activation of immunological cytotoxic pathways.

Animals↗
PubMed1975

[The lymphocyte cytotoxicity test in tumor immunology (author's transl)].

The cytotoxic action of lymphocytes on cancer cells in vitro indicates sensitization of the patient against his own tumor. The technical difficulities of this test and possibilities of standardization and simplifying the procedure are discussed. Critical steps are isolation of lymphocytes and culturing target cells without loosing their specific antigenic structure. The need for specificity controls both for lymphocytes and tumor cells is emphasized. Labelling tumor cells with isotopes represents a major improvement in evaluating the result. The role of thymus- and bone marrow-dependent lymphocytes as well as blocking factors in the serum of tumor patients can be analyzed in the cytotoxic assay. A better understanding of these mechanisms may facilitate a therapeutic approach by manipulating the interaction of tumor cells and host.

Animals↗
PubMed1978

Immunopathologic studies of rheumatoid arthritis. I. Absence of complement-dependent cytotoxicity of rheumatoid sera for rheumatoid synovial cell cultures.

A sensitive complement-dependent chromium release cytotoxicity assay was used to determine whether sera from rheumatoid arthritis (RA) patients contain antibody specific for an antigen on rheumatoid synovial cell cultures. Two hundred eight RA sera-RA synovial culture combinations were studied employing 21 sera and 16 synovial membranes; control combinations were derived from 5 normal sera and 10 degenerative joint disease synovial membranes. Anticomplementary activity of some rheumatoid sera was overcome using an increased complement concentration. The percent cytotoxicity of RA serum-RA culture combinations, both homologous and autologous, was not significantly greater than that of RA serum-control culture combinations. No correlation between duration of disease or duration of cell culture and percent cytotoxicity was found. Thus a unique antigen on cultured rheumatoid synovial cells was not recognized by rheumatoid serum antibody by use of this cytotoxicity assay.

Adolescent↗
PubMed1978

Colony formation of cytolytic T cells in semisolid medium.

Addition of supernatant from concanavalin A-stimulated spleen cells to in vitro primed cytolytic T lymphocytes in semisolid medium stimulated the growth of colonies of cytolytic lymphocytes. Optimal results were obtained using a peritoneal adherent cell underlayer where a 10% plating efficiency (greater than or equal to 4 cells per colony) was achieved when between 5000 and 100 000 cells were plated per dish. Individual colonies were harvested and tested in a short term (5h) 51Cr release microassay, employing 200 target cells. The frequency of lytic colonies varied from 46--67%. The observed lytic activities were specific for the relevant allogeneic target cells.

Animals↗
PubMed1978

Influenza virus-specific cytotoxic T cells in man; induction and properties of the cytotoxic cell.

Human peripheral blood lymphocytes have been sensitized in vitro to influenza virus antigen. After an induction period of 4--14 days, cytotoxic cells which lyse autologous influenza virus-infected lymphoid cells could be demonstrated. The cytotoxic cell is a T lymphocyte which shows specificity for sensitizing influenza virus type A or B. It cannot distinguish between major subtypes of influenza A virus. The use of virus-infected normal lymphoid cells as target cells overcame the difficulties of nonspecific killing encountered with some transformed cells.

Cytotoxicity Tests, Immunologic↗
PubMed1979

High nonspecific reactivity of normal lymphocytes against mycoplasma-infected target cells in cytotoxicity assays.

Several rat tumor cell cultures were deliberately infected with three species of mycoplasma commonly found as contaminants of cell lines grown in vitro, and the effect of mycoplasma infection on the results of cytotoxicity assays was examined. Lymph node cells and spleen cells from normal animals showed an apparently high spontaneous cytotoxic activity against tumor cells infected with either M. arginini or M. hyorhinis, but the reactivity against cells infected with M. orale was not significantly higher than that against uninfected cells. The high reactivity towards tumor cells infected with M. arginini and M. hyorhinis bore a close resemblence to natural cell-mediated immunity in that spleen cells were much more reactive than lymph node cells, spleen cells from nude mice were as effective as spleen cells from normal mice, and the reaction crossed both strain and species barriers. However, closer examination revealed that the cytotoxic effects were directly caused by depletion of arginine or other essential nutrients from the medium. These findings imply that a cautious approach should be taken when interpreting certain aspects of spontaneous cell-mediated cytotoxicity, and that the greatest care be taken to ensure that the cells used as targets in any cytotoxicity test are mycoplasma-free.

Animals↗
PubMed1977

Tumor-associated humoral cytotoxicity in patients with acute myelogenous leukemia before and after chemotherapy.

Sera of eight unselected adult patients with acute myelogenous leukemia obtained before and after chemotherapy were repeatedly tested for specific complement-dependent cytotoxicity against autochthonous peripheral white blood cells from the acute leukemia stage and from the remission stage, respectively. Complement-dependent cytotas demonstrated in all of the eight patients, while none of three patients' sera were reactive against white blood cells from the remission stage tested in parallel. The cytotoxicity was increased after chemotherapy, also in those patients in whom remission was not achieved.

Adult↗
PubMed1978

Human natural cytotoxicity in the blood and lymphoid organs of healthy donors and patients with malignant disease.

Natural cytotoxicity against CLA-4 and D6 target cells was determined in the peripheral blood of healthy donors and women with mammary carcinoma (localized to the breast and axilla), and in human normal and regional tumour lymph nodes. The NK cell activity in the blood of women with clinically localized mammary carcinoma showed a wide range of reactivities but was similar to the pattern detected in healthy controls. The NK cell activity in human normal lymph nodes also showed a wide range and was the same irrespective of the anatomical site of origin of the lymph node. Lymph nodes draining a variety of solid tumours had a similar spectrum of NK cell activity, there being no obvious correlation between the level of NK cell activity and such parameters as size and histological type of tumour, hyperplasia or metastatic spread in the regional node. Trypsin treatment of lymphocyte suspensions from the various lymphoid compartments suggested that the cell responsible for natural cytotoxicity in blood was probably different from the NK cell in tonsil and lymph nodes.

Adult↗
PubMed1978

Characterization of the human natural killer (NK) cell in blood and lymphoid organs.

The human natural killer (NK) cell in peripheral blood is a non-thymus-dependent, (Fc+ C3-), Ig-bearing lymphocyte and is probably identical to the human K cell, although not requiring the Fc receptor, in contrast to the K cell, for the lytic process. The human NK cell in tonsil and lymph node, on the other hand, is a non-Ig- bearing T lymphocyte, lacking both Fc and C3 receptors.

Cell Migration Inhibition↗
PubMed1978

Studies of effector cell, antibody, and target cell interactions in natural cell-mediated cytotoxicity.

IgG antibodies bound to effector cells through Fc receptors were observed to determine the specificity of natural cell-mediated cytotoxicity (NCMC) against cultured target cells. When effector lymphocytes were isolated from the peripheral blood of most individuals, they already possessed natural antibodies specific for antigens on cultured cells. Since they lacked IgG antibodies specific for antigens on sheep red blood cell (SRBC) targets, natural cytotoxicity against SRBC was almost non-existent. Effector cells incubated in IgG anti-SRBC became specifically cytotoxic to SRBC. In the process, NCMC and antibody-dependent cell-mediated cytotoxicity was diminished, indicating that arming with anti-SRBC replaced natural antibodies and occupied Fc receptors on effector cells. Thus, treating effector cells with serum may result in increased or decreased cytotoxicity depending upon the specificity of antibodies within the serum. This type of modulation of NCMC occurs at the interaction between antibody Fc and Fc receptors and can explain blocking and unblocking.

Animals↗
PubMed1979

Cell-mediated reactivity to antigens shared by Moloney-virus-induced lymphomas (LSTRA) and certain 3-methylcholanthrene-induced mouse sarcomas.

Spleen cells (SC) both from BALB/c mice whose primary Moloney sarcoma virus (MSV)-induced sarcomas had spontaneously regressed and from normal, untreated BALB/c mice, were co-cultivated for 5 days with mitomycin-C-treated LSTRA cells; LSTRA is a BALB/c Moloney lymphoma which shares cell surface antigens with MSV-indiced sarcomas. These SC, referred to as CMR and CU cells, respectively, were shown to be cytotoxic to LSTRA cells in 3 h 51Cr-release assays; CMR cells showed, in most cases, the greatest lytic activity against LSTRA targets. The same SC were also reactive, in 20-h microcytotoxicity and 51Crassays, against target cells from a variety of transplanted sarcomas indiced by 3-methylcholanthrene (MCA) in Balb/c mice. The highest reactivity was seen when CMR or CU cells were tested against target cells from sarcoma lines that expressed an NB-ecotropic MuLV cross-reacting serologically with Moloney virus. Reactivity against isotope-labelled tumor cells expressing MuLV-associated cell surface antigens could be competititively inhibited by adding unlabelled tumor cells expressing such antigens. Finally, Winn assays were performed in which CMR cells strongly inhibited the outgrowth of cells from three sarcoma lines that express the NB-ecotropic MuLV. There was less but significant inhibition of cells from some other MCA sarcomas, either negative for the expression of MuLV-associated antigens or expressing the N-ecotropic endogenous BALB/c MuLV. CU cells enhanced tumor outgrowth in Winn assays at least as often as they inhibited it.

Animals↗
PubMed1979

Cell-mediated cytotoxicity for cultured autologous melanoma cells.

Peripheral blood lymphocytes from 32 patients with malignant melanoma were tested for cell-mediated cytotoxicity (CMC) against cultured autologous melanoma cells. Effector cells were prepared from venous blood by defibrination, gel sedimentation, nylon column filtration, and lysis of remaining erythrocytes with NH4Cl. Melanoma cells prelabelled with [3H])proline were used as target cells in a 40-h assay and CMC was evaluated against standards obtained with blood lymphocytes from the least reactive normal donor. Reproducible autologous CMC was detected in 18 of 32 patients in a series of 367 total tests. CMC correlated with tumor volume (5-500 cm3) but not with tumor stage or DNCB reactivity. Preliminary results indicated that autologous CMC was not affected by treatment with DTIC, dexamethasone, intralesional BCG, radiation therapy, or partial surgical excision. Lack of consistent CMC in 14 patients could not be attributed to a measurable decrease in general immune capacity or to increased resistance of the patients' melanoma cells to CMC in general. Fibroblasts were more resistant to CMC than melanoma cells, and therefore of questionable value for defining specificity in direct tests.

Adult↗
PubMed1979

Decreased cell-mediated cytotoxicity against virus-infected cells in systemic lupus erythematosus.

Cell-mediated cytotoxicity, directed against virus-infected tissue culture cells, was studied with peripheral blood mononuclear cells from 11 patients with systemic lupus erythematosus (SLE) and 12 matched, normal subjects in a 51Cr release assay. Baseline (preimmunization) levels of cytotoxicity against target cells infected with influenza A/Victoria, influenza B/Hong Kong, Newcastle disease virus, and herpes simplex virus were significantly decreased in patients with SLE compared to normal subjects (P less than 0.001), although serum antibody levels to the respective viruses were similar in both groups. After intramuscular administration of inactivated influenza A/Victoria vaccine, SLE patients failed to generate elevated levels of cytotoxicity against A/Victoria-infected cells, in contrast to normal subjects. SLE patients responded with levels of serum hemagglutination-inhibition antibody which were similar to those of normal subjects. Thus, SLE patients manifest decreased cell-mediated cytotoxicity against virus-infected target cells, although humoral antibody responses appeared to be intact. Studies of SLE patients with influenza may help to define the role of cell-mediated immunity in the pathogenesis of certain viral infections.

Adolescent↗