scholarly journals Growth-inhibitory activity of lymphoid cell plasma membranes. I. Inhibition of lymphocyte and lymphoid tumor cell growth.

1984 ◽  
Vol 99 (4) ◽  
pp. 1221-1226 ◽  
Author(s):  
K C Stallcup ◽  
A Dawson ◽  
M F Mescher
Keyword(s):  
Plasma Membrane ◽  
Tumor Cell ◽  
Growth Inhibition ◽  
Tumor Cells ◽  
Inhibitory Activity ◽  
Calf Serum ◽  
Lymphoid Cells ◽  
Spleen Cells ◽  
Lymphoid Tumor ◽  
Normal Spleen

Membranes isolated from normal spleen cells or lymphoid tumor cells were found to inhibit in vitro growth of several murine tumor cell lines including a B cell hybridoma, a thymoma, and a mastocytoma. 50% inhibition occurred at membrane protein concentrations of 60-100 micrograms/ml. A similar concentration dependence was found for inhibition of [3H]-thymidine incorporation by tumor cells and for the lipopolysaccharide-induced mitogenic response of normal spleen cells. The inhibitory activity co-purified with the plasma membrane upon fractionation of crude membranes. Membrane solubilization with deoxycholate followed by dialysis to remove the detergent gave good recovery of inhibitory activity in the resulting reconstituted membranes. Membrane-mediated growth inhibition resulted from a decreased rate of proliferation and not from increased cell death. A toxic effect of the membranes was further ruled out by the finding that increasing the fetal calf serum content of the medium could substantially reverse the growth inhibition. Thus, the plasma membrane of lymphoid cells contains a component that can slow or stop the growth of cells in culture. This membrane component may have a role in cell contact-mediated regulation of growth.

Inhibition of lymphocyte responsiveness by a glial tumor cell-derived suppressive factor

1987 ◽  
Vol 67 (6) ◽  
pp. 874-879 ◽  
Author(s):  
Thomas L. Roszman ◽  
William H. Brooks ◽  
Lucinda H. Elliott
Keyword(s):  
Tumor Cell ◽  
Tumor Cells ◽  
Human Peripheral Blood ◽  
Calf Serum ◽  
Lymphocyte Activation ◽  
Peripheral Blood Lymphocytes ◽  
Prostaglandin E ◽  
Suppressive Activity ◽  
Glial Tumor ◽  
Culture Supernatants

✓ The results of this study demonstrate the presence of suppressive factor(s) in the tissue culture supernatants of cloned and freshly explanted malignant glioma cells. Culture supernatants obtained from these glial cell lines were demonstrated to have potent suppressive activity as evidenced by their ability to inhibit the proliferative response of normal human peripheral blood lymphocytes induced by phytohemagglutinin and anti-OKT3 monoclonal antibodies. The results further demonstrate the existence of a dose-response relationship between these supernatants and inhibition of mitogen-induced lymphocyte activation. Maximum production of suppressive activity by glial tumor cells was dependent on: 1) the number of tumor cells seeded in culture, 2) whether fetal calf serum was present, and 3) the duration of culture. The production of the suppressive factor(s) was not inhibited by the addition of inhibitors of prostaglandin E synthesis. Experiments designed to determine at what time during lymphocyte activation the suppressive factor was most effective demonstrated that the culture supernatants must be added during the first 24 hours of culture to exhibit inhibitory properties. Finally, proliferation of both the T-helper and T-suppressor/cytotoxic subsets was equally well inhibited by the glial tumor cell culture supernatants.

Hypoxia-activated ligand HAL-1/13 is lupus autoantigen Ku80 and mediates lymphoid cell adhesion in vitro

2001 ◽  
Vol 280 (4) ◽  
pp. C897-C911 ◽  
Author(s):  
Eileen M. Lynch ◽  
Robert B. Moreland ◽  
Irene Ginis ◽  
Susan P. Perrine ◽  
Douglas V. Faller
Keyword(s):  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Lines ◽  
Lymphoid Cell ◽  
Ectopic Expression ◽  
Lymphoid Cells ◽  
Expression Cloning ◽  
Hypoxic Exposure ◽  
Tumor Cell Lines ◽  
Human Lymphoid Cell

Hypoxia is known to induce extravasation of lymphocytes and leukocytes during ischemic injury and increase the metastatic potential of malignant lymphoid cells. We have recently identified a new adhesion molecule, hypoxia-activated ligand-1/13 (HAL-1/13), that mediates the hypoxia-induced increases in lymphocyte and neutrophil adhesion to endothelium and hypoxia-mediated invasion of endothelial cell monolayers by tumor cells. In this report, we used expression cloning to identify this molecule as the lupus antigen and DNA-dependent protein kinase-associated nuclear protein, Ku80. The HAL-1/13-Ku80 antigen is present on the surface of leukemic and solid tumor cell lines, including T and B lymphomas, myeloid leukemias, neuroblastoma, rhabdomyosarcoma, and breast carcinoma cells. Transfection and ectopic expression of HAL-1/13-Ku80 on (murine) NIH/3T3 fibroblasts confers the ability of these normally nonadhesive cells to bind to a variety of human lymphoid cell lines. This adhesion can be specifically blocked by HAL-1/13 or Ku80-neutralizing antibodies. Loss of expression variants of these transfectants simultaneously lost their adhesive properties toward human lymphoid cells. Hypoxic exposure of tumor cell lines resulted in upregulation of HAL-1/13-Ku80 expression at the cell surface, mediated by redistribution of the antigen from the nucleus. These studies indicate that the HAL-1/13-Ku80 molecule may mediate, in part, the hypoxia-induced adhesion of lymphocytes, leukocytes, and tumor cells.

scholarly journals CELL TO CELL INTERACTION IN THE IMMUNE RESPONSE

1968 ◽  
Vol 128 (4) ◽  
pp. 855-874 ◽  
Author(s):  
W. J. Martin ◽  
J. F. A. P. Miller
Keyword(s):  
Immune Response ◽  
Cell Interaction ◽  
Lymphoid Cells ◽  
Target Cells ◽  
Antilymphocyte Globulin ◽  
Spleen Cells ◽  
Sheep Erythrocytes ◽  
Normal Spleen ◽  
Thymus Cells

In this series of papers it has been shown that the immune response of mice to sheep erythrocytes requires the participation of two classes of lymphoid cells. Thymus-derived cells initially react with antigen and then interact with another class of cells, the antibody-forming cell precursors, to cause their differentiation to antibody-forming cells. Antilymphocyte globulin depressed the ability of mice to respond to sheep erythrocytes. This effect was more marked when the antigen was injected intraperitoneally than intravenously, and occurred only when the antilymphocyte globulin was given before or simultaneously with antigen. Injection of thymus cells restored to near normal the ability to respond to an intravenous injection of sheep erythrocytes. Spleen cells from antilymphocyte globulin-treated mice gave a weak adoptive immune response in irradiated recipients. The addition of thymus cells however enabled a response similar to that given by normal spleen cells. When thymectomized irradiated recipients were used, normal spleen cells continued to give a higher response to a challenge of sheep erythrocytes at 2 and 4 wk postirradiation than did spleen cells from ALG-treated donors. This result is more consistent with the notion that thymus-derived target cells are eliminated, rather than temporarily inactivated, by antilymphocyte globulin. These findings suggest that, in vivo, antilymphocyte globulin acts selectively on the thymus-derived antigen-reactive cells.

scholarly journals STIMULATION OF ANTIBODY PRODUCTION TO THE HAPTEN 2,4-DINITROBENZENE BY AFFINITY LABELED MURINE LYMPHOID CELLS

1974 ◽  
Vol 139 (4) ◽  
pp. 943-956 ◽  
Author(s):  
David A. Lawrence ◽  
William O. Weigle
Keyword(s):  
Immune Response ◽  
B Cells ◽  
Lymphoid Cells ◽  
Cellular Interaction ◽  
Cell Populations ◽  
Cell Contact ◽  
Spleen Cells ◽  
Normal Spleen ◽  
Thymus Cells

The ability of meta-nitrobenzenediazonium fluoborate (m-NBDF)-labeled thymus and spleen (S) cells to transfer immunity to 2,4-dinitrophenyl (DNP) into irradiated syngeneic recipients was investigated. There was a significant increase in the number of anti-DNP plaque-forming cells (PFC) when m-NBDF-labeled thymus cells and normal spleen cells, or normal thymus cells and m-NBDF-labeled spleen cells were transferred, but not when both thymus- and S-cell populations were labeled and injected together into irradiated recipients. The ability of these cell populations to cooperate and enhance the in vivo immune response to DNP is discussed. The T cells seem to be actively involved in the development of this response; they participate beyond the mere role of carrying and presenting antigen to the B cells. It is suggested that cell to cell contact between T and B cells may be an important factor in the elicitation of an immune response. In addition, the cellular interaction is affected by irradiating the thymus cell preparation and the initiating interaction required for antibody synthesis probably occurs within 48 h after injecting the cell populations into the syngeneic irradiated recipients.

scholarly journals Cross-reactive lysis of trinitrophenyl (TNP)-derivatized H-2 incompatible target cells by cytolytic T lymphocytes generated against syngeneic TNP spleen cells.

1976 ◽  
Vol 144 (6) ◽  
pp. 1609-1620 ◽  
Author(s):  
S J Burakoff ◽  
R N Germain ◽  
B Benacerraf
Keyword(s):  
T Lymphocytes ◽  
Red Blood Cells ◽  
Target Cell ◽  
Blood Cells ◽  
Surface Antigens ◽  
Lymphoid Cells ◽  
Target Cells ◽  
Cytolytic T Lymphocytes ◽  
Spleen Cells ◽  
Normal Spleen

Normal spleen cells, when cultured with irradiated trinitrophenyl (TNP)-derivatized syngeneic spleen cells, develop cytotoxic effectors that lyse most effectiviely a TNP-derivatized target that is H-2 compatible with the effector. However, these effectors also lyse to a lesser extent TNP tumor and TNP spleen targets that are H-2 incompatible. This cross-reactive lysis correlates with the degree of cytolysis seen on the TNP-derivatized syngeneic target; it appears to be medicated by Thy 1.2-bearing cells and is inhibited by antisera to the K and/or D loci of the target cell and not by antisera to non-K or non-D surface antigens. Nonradiolabeled TNP-derivatized lymphoid cells syngeneic to either the stimulator or the target are able to competitively inhibit cross-reactive lysis, while TNP chicken red blood cells are unable to specifically inhibit lysis. These data on cross-reactive lysis of TNP-conjugated targets are most consistent with the altered-self hypothesis.

scholarly journals INCREASED REACTIVITY OF MOUSE SPLEEN CELLS SENSITIZED IN VITRO AGAINST SYNGENEIC TUMOR CELLS IN THE PRESENCE OF A THYMIC HUMORAL FACTOR

1973 ◽  
Vol 138 (6) ◽  
pp. 1521-1532 ◽  
Author(s):  
Claude Carnaud ◽  
David Ilfeld ◽  
Itzhak Brook ◽  
Nathan Trainin
Keyword(s):  
Tumor Cells ◽  
Culture Media ◽  
Lymphoid Cells ◽  
Humoral Factor ◽  
Mouse Spleen ◽  
Spleen Cells ◽  
Effector Phase ◽  
Syngeneic Tumor ◽  
Mediate Cytotoxicity

Unprimed mouse spleen cells cultured in vitro on syngeneic tumor cell monolayers have been previously shown to become specifically sensitized and to mediate cytotoxicity against the same type of tumor cells. This complete in vitro system of cell-mediated response has been presently used to test the effect of a thymic humoral factor (THF) upon the differentiation process leading to the generation of specifically committed lymphocytes. Culture media were supplemented with 2% THF during either the sensitization or effector phase, or both phases of the reaction. Whereas the addition of THF during both phases or during sensitization only resulted in a significant increase in the cytotoxicity index, THF added during the effector phase was ineffective. The behavior of unsensitized spleen cells and of spleen cells sensitized against nonrelated transplantation antigens remained unmodified by THF. After showing that the entire reaction is mediated by lymphocytes of thymic origin, THF was directly tested on T or B spleen cells. It was found that only T cells reacted to THF by an increased cytotoxic capacity, while B cells remained inactive after addition of THF. It was therefore concluded that THF activates a postthymic population of lymphoid cells, transforming them into fully competent lymphocytes.

scholarly journals A diffusible stimulator of eosinophilopoiesis produced by lymphoid cells as demonstrated with diffusion chambers

Blood ◽  
1976 ◽  
Vol 48 (2) ◽  
pp. 293-300
Author(s):  
AM Miller ◽  
MP McGarry
Keyword(s):  
Bone Marrow Cells ◽  
Marrow Cell ◽  
Diffusion Chamber ◽  
Lymphoid Cells ◽  
Spleen Cells ◽  
Secondary Challenge ◽  
Normal Spleen ◽  
A Cell ◽  
Marrow Cellularity

Previous experiments have indicated that eosinophilopoiesis is stimulated in lymphoid cell-dependent eosinophil responses to certain antigens. In order to study if the potential for this stimulation of eosinophilopoiesis is a function of lymphoid cells and can be expressed on challenge with the eosinophilia-inducing antigen, the diffusion chamber technique for the culture in vivo of murine hemopoietic cells has been modified. A quadrachamber diffusion assembly allows for the simultaneous maintenance in the same host of four cell populations, pairs of which are separated by a cell-impermeable Millipore diffusion membrane of defined porosity. Spleen cells for chambers were from normal mice and mice primed with tetanus toxoid; secondary challenge induces eosinophilia. These spleen cells were placed transfilter from isogeneic bone marrow cells and cultured in vivo for 6 days in normal mice that received tetanus toxoidintraperitoneally following chamber- assembly implant. The marrow cell transfilter from spleen cells of primed-donor origin exhibited significantly greater eosinophilopoiesis than contiguous-chamber marrow transfilter from normal spleen cells. Such stimulated eosinophilopoiesis was independent of total chamber marrow cellularity. The data indicated that antigen-stimulated lymphoid cells may be the source of an eosinophilopoietic factor.

Expression of bovine coronavirus antigens at the plasma membrane in infected cell cultures

1987 ◽  
Vol 45 ◽  
pp. 930-931
Author(s):  
H. R. Payne
Keyword(s):  
Plasma Membrane ◽  
Culture Medium ◽  
Calf Serum ◽  
Spleen Cells ◽  
Adenocarcinoma Cell Line ◽  
Bovine Coronavirus ◽  
Severe Diarrhea ◽  
Intracellular Compartments ◽  
Host Plasma Membrane ◽  
Neonatal Calves

Infection by bovine coronavirus (BCV) may cause severe diarrhea in neonatal calves. The virus can multiply in the human adenocarcinoma cell line HRT-18 and in bovine fetal spleen cells (BFS). Fusion of BFS cells occurs after BCV infection if trypsin is added to the culture medium. This type of fusion may be induced by other enveloped viruses following the expression of virally encoded macromolecules in the plasma membrane. The presence of viral proteins in the host plasma membrane is not, however, necessary for BCV maturation since coronaviral particles are enveloped by budding into intracellular compartments. Immunogold techniques were used to determine if BCV proteins are present in the plasma membrane of the host cell and whether their absence might explain the lack of fusion in BFS cells not treated with trypsin.Monolayers of HRT-18 cells, grown in DMEM medium with 5% fetal calf serum, were infected with BCV.

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