scholarly journals Role of activated macrophages in antibody-dependent lysis of tumor cells.

1980 ◽  
Vol 152 (1) ◽  
pp. 183-197 ◽  
Author(s):  
C Nathan ◽  
L Brukner ◽  
G Kaplan ◽  
J Unkeless ◽  
Z Cohn
Keyword(s):  
Tumor Cells ◽  
Peritoneal Macrophages ◽  
Activated Macrophages ◽  
Fab Fragment ◽  
Bacille Calmette Guerin ◽  
Pharmacologic Agent ◽  
Peritoneal Cells ◽  
Specific Contact ◽  
Cytolytic Response

Treatment of mice with Bacille Calmette-Guérin (BCG) or C parvum activates their peritoneal macrophages to release increased amounts of H2O2, and thereby to lyse extracellular tumor cells, in response to a pharmacologic agent, phorbol myristate acetate (PMA) (1-3). In the present study, the same bacterial vaccines activated peritoneal cells to become cytolytic to lymphoma cells sensitized with alloantiserum, in the absence of PMA. Resident peritoneal cells, or those elicited with thioglycollate broth, were ineffective, not only in PMA-induced lysis, but also in antibody-dependent lysis of tumor cells. The cytolytic effect of BCG peritoneal cells toward sensitized tumor cells appeared to be mediated mostly by macrophages. Cytotoxicity was immunologically specific, contact dependent, rapid, and efficient. Phagocytosis of intact tumor cells was not involved. Alloantiserum-dependent cytolysis was specifically blocked by the Fab fragment of a monoclonal antibody directed against the trypsin-resistant macrophage Fc receptor (FcR II). Thus, tumor cells coated with homologous immunoglobulin interact with FcR II on activated macrophages to trigger an extra-cellular cytolytic response.

Role of interferon-activated macrophages in eradication of human tumor cells by innate immunity

Cytokine ◽  
2009 ◽  
Vol 48 (1-2) ◽  
pp. 48
Author(s):  
Samuel Baron ◽  
Julie Horowitz ◽  
Joyce Poast ◽  
Angel Morrow ◽  
Samuel Fey ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Tumor Cells ◽  
Human Tumor ◽  
Activated Macrophages ◽  
Human Tumor Cells

scholarly journals Bacille Calmette-Guérin infection in the mouse. Regulation of macrophage plasminogen activator by T lymphocytes and specific antigen.

1978 ◽  
Vol 147 (4) ◽  
pp. 1175-1188 ◽  
Author(s):  
S Gordon ◽  
Z A Cohn
Keyword(s):  
T Lymphocytes ◽  
Plasminogen Activator ◽  
Macrophage Activation ◽  
Specific Antigen ◽  
Peritoneal Macrophages ◽  
Bacille Calmette Guerin ◽  
Vitro Assay ◽  
Purified Protein Derivative ◽  
Peritoneal Cells

High levels of plasminogen activator (PA) were induced in mouse peritoneal macrophages by infection with BCG, 2-6 X 10(7) viable organisms intravenously, followed 3-4 wk later by intraperitoneal challenge with purified protein derivative (PPD) 2 days before harvest. Macrophages obtained from infected animal without boosting showed little fibrinolytic activity, but challenge of Bacille-Calmette-Guèrin (BCG)-primed peritoneal cells with PPD in culture also enhanced macrophage PA 4- to 10-fold. Stimulation of macrophage PA by PPD depended on specifically sensitized thymus-derived (T) lymphocytes because it was abolished by pretreatment of BCG-primed peritoneal cells with anti-thy 1.2 antiserum and complement. A direct assay was developed in which nylon wool separated sensitized lymphocytes and PPD induced PA in macrophages from uninfected animals under defined conditions on 125I-fibrin. Enhanced macrophage fibrinolysis was proportional to concentration of PPD and the number of sensitized lymphocytes transferred. An indirect two-stage assay was also used to show that BCG-sensitized peritoneal cells released a soluble inducer of macrophage PA into the culture medium, after challenge with PPD. Induction of macrophage PA by PPD challenge in vitro made it possible to study the generation and activity of sensitized peritoneal lymphocytes at different stages of infection. Our results show that nonadherent peritoneal cells of BCG-infected mice provide a rich source of specifically sensitized lymphocytes and that macrophage activation is limited by continued availability of antigen, as well as sensitized lymphocytes. Induction of macrophage PA provides a sensitive, versatile, and rapid in vitro assay to study the role of lymphocytes and specific antigen in macrophage activation by BCG.

scholarly journals Role of oxygen-dependent mechanisms in antibody-induced lysis of tumor cells by activated macrophages

1980 ◽  
Vol 152 (1) ◽  
pp. 198-208 ◽  
Author(s):  
C Nathan ◽  
Z Cohn
Keyword(s):  
Hydrogen Peroxide ◽  
Cytochalasin B ◽  
Starch Granules ◽  
Activated Macrophages ◽  
Myristate Acetate ◽  
Lymphoma Cells ◽  
Bacille Calmette Guerin ◽  
Effector Cells ◽  
Hydrogen Peroxide Release

The alloantiserum-dependent lysis of TLX9 lymphoma cells by peritoneal cells from Bacille Calmette-Guerin (BCG)-treated mice was inhibited 62 percent by depletion of oxygen. This effect did not appear to be a result of interference with mitochondrial respiration because cyanide, azide, and dinitrophenol did not inhibit cytotoxicity. Preincubating the effector cells for 2 h without glucose, which markedly reduces their ability to release hydrogen peroxide, likewise suppressed antibody-dependent cytolysis by 62 percent. Lysis of sensitized lymphoma cells was virtually abolished by 6 mg/ml of thioglycollate broth, a concentration that also abrogated the detectable release of hydrogen peroxide and the lysis of lymphoma cells by BCG-activated macrophages in response to phorbol myristate acetate (PMA). This concentration of thioglycollate broth was not toxic to the effector cells, as judged by adherence to plastic, binding of opsonized erythrocytes, and phagocytosis of radiolabeled starch granules. Catalase, superoxide dismutase, horseradish peroxidase, mannitol, ethanol, benzoate, and diazabicyclooctane were without consistent effects. Cytochalasin B and dihydrocytochalasin B both markedly suppressed cytolysis, whether induced by antibody or by PMA (ID(50), 0.5 μg/ml). Cytoehalasin B was an equally potent suppressor of glucose uptake and PMA-induced hydrogen peroxide release by BCG-activated macrophages (ID(50), 0.5 μg/ml). However, dihydrocytochalasin B lacked these latter effects, which suggests that cytotoxicity required intact contractile elements. The extracellular lysis of antibody-coated lymphoma cells by BCG-activated macrophages appears to have a predominantly oxidative basis.

scholarly journals The pinocytic rate of activated macrophages.

1975 ◽  
Vol 142 (5) ◽  
pp. 1150-1164 ◽  
Author(s):  
P J Edelson ◽  
R Zwiebel ◽  
Z A Cohn
Keyword(s):  
Horseradish Peroxidase ◽  
Concanavalin A ◽  
Peritoneal Macrophages ◽  
Intermediate Level ◽  
Cell Protein ◽  
Activated Macrophages ◽  
Peritoneal Cells ◽  
Activated State ◽  
Sustained Increase

Peritoneal macrophages from mice injected 4 days previously with Brewer's thioglycollate medium have a pinocytic rate, in culture, of 190 ng horseradish peroxidase (HRP)/100 mug cell protein/h, compared to the rate of resident peritoneal cells of 53 ng HRP/100 mug cell protein/h. Mice injected with endotoxin or with only certain of the components of the Brewer's medium show an intermediate level of stimulation. The rate of unstimulated, endotoxin-stimulated, or thioglycollate-stimulated cells shows little change over several days in culture. The pinocytic rate of thioglycollate-stimulated cells can, however, be further increased by exposure of concanavalin A. Although cells may show transient increases in their pinocytic rate in many situations, a sustained increase in pinocytic rate is a sign of the "activated" state of macrophages.

scholarly journals Leukocyte subpopulations elicited by a nontumorigenic variant of B16 melanoma: their role in direct rejection of the melanoma and in prevention of tumorigenesis in Winn assays.

1982 ◽  
Vol 156 (6) ◽  
pp. 1723-1738 ◽  
Author(s):  
T A Calvelli ◽  
V H Freedman ◽  
S C Silverstein ◽  
S Silagi
Keyword(s):  
Tumor Cells ◽  
Cell Function ◽  
Peritoneal Macrophages ◽  
Tumor Formation ◽  
B16 Melanoma ◽  
Tumoricidal Activity ◽  
Peritoneal Cells ◽  
Peritoneal Leukocytes ◽  
Leukocyte Populations

The mechanisms by which various leukocyte subpopulations elicited by an immunogenic, nontumorigenic subclone (C3471) of B16 melanoma caused rejection of the tumorigenic parental melanoma (B559), were investigated. Leukocytes from C3471-immune mice were co-injected with B559 tumor cells in Winn assays into normal syngeneic recipients. Tumor formation by B559 cells was prevented when C3471-immune (a) unfractionated peritoneal leukocytes, or (b) glass-adherent peritoneal cells (90% macrophages), or (c) nylon wool purified nonadherent cells (95% Thy-1.2+) were used in the Winn assays. If the C3471-immunized mice were treated with antithymocyte serum before harvest of their peritoneal cells, none of these leukocyte populations were effective in the Winn assay. However, macrophages from these immunologically compromised donors regained their tumoricidal activity after incubation in vitro with T lymphocytes from untreated C3471-immune donors; similarly, C3471-immune lymphocytes rendered normal resident peritoneal macrophages tumoricidal in Winn assays. When C3471-immunized mice were irradiated or treated with antithymocyte serum before direct challenge with B559 cells, melanomas developed, thus providing additional evidence for the need for intact T cell function to establish immunity against the melanoma. Furthermore, when Winn assay recipients were treated with antithymocyte serum, neither C3471-immune macrophages nor T cells were able to prevent tumor formation. These findings indicate that antithymocyte serum-sensitive (Thy-1.2+) lymphocytes are necessary both for the generation of tumoricidal leukocytes in C3471-immunized mice, and for the rejection of B559 melanoma by demonstrably tumoricidal macrophages in Winn assay recipients. In addition, long-lasting immunity developed in 50% of the normal mice that had received both C3471-immune peritoneal cells and B559 tumor cells, as manifested by their capacity to reject a second challenge with B559 cells 40-60 d later.

The Role of the Interaction between Fe(III) and Cell Surface in the Accumulation of 67Ga by Tumor Cells

1991 ◽  
Vol 30 (06) ◽  
pp. 290-293 ◽  
Author(s):  
P. Maleki ◽  
A. Martinezi ◽  
M. C. Crone-Escanye ◽  
J. Robert ◽  
L. J. Anghileri
Keyword(s):  
Cell Surface ◽  
Tumor Cells ◽  
Ionic Composition ◽  
Iron Complex ◽  
Iron Binding ◽  
Complex Time ◽  
Interaction Product ◽  
Thermodynamic Constant ◽  
Number Of Cells

The study of the interaction between complexed iron and tumor cells in the presence of 67Ga-citrate indicates that a phenomenon of iron-binding related to the thermodynamic constant of stability of the iron complex, and a hydrolysis (or anion penetration) of the interaction product determine the uptake of 67Ga. The effects of various parameters such as ionic composition of the medium, nature of the iron complex, time of incubation and number of cells are discussed.

Role of exosomes in diagnosis and therapy of prostate cancer

2020 ◽  
Vol 28 (3) ◽  
pp. 399-405
Author(s):  
Fabrizio Fontana ◽  
Olga A. Babenko
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Biological Fluids ◽  
Diagnosis And Treatment ◽  
Diagnosis And Therapy ◽  
The Future ◽  
Important Direction ◽  
Potential Biomarkers

Aim of this letter is to attract the attention of journal readers to the study of exosomes as an important direction in the development of Oncology, in particular, in the diagnosis and treatment of prostate cancer. Exosomes are produced by tumor cells and regulate proliferation, metastasis, and the development of chemoresistance. Their extraction from biological fluids allows further use of these vesicles as potential biomarkers of prostate cancer. In the future, exosomes can be successfully used in the delivery of drugs and other anti-tumor substances to cancer cells.

The Role of Reactive Oxygen Species in Tumor Treatment and its Impact on Bone Marrow Hematopoiesis

2020 ◽  
Vol 21 (5) ◽  
pp. 477-498
Author(s):  
Yongfeng Chen ◽  
Xingjing Luo ◽  
Zhenyou Zou ◽  
Yong Liang
Keyword(s):  
Reactive Oxygen Species ◽  
Bone Marrow ◽  
Oxidative Damage ◽  
Tumor Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tumor Treatment ◽  
Normal Cells ◽  
Treatment And Prevention

Reactive oxygen species (ROS), an important molecule inducing oxidative stress in organisms, play a key role in tumorigenesis, tumor progression and recurrence. Recent findings on ROS have shown that ROS can be used to treat cancer as they accelerate the death of tumor cells. At present, pro-oxidant drugs that are intended to increase ROS levels of the tumor cells have been widely used in the clinic. However, ROS are a double-edged sword in the treatment of tumors. High levels of ROS induce not only the death of tumor cells but also oxidative damage to normal cells, especially bone marrow hemopoietic cells, which leads to bone marrow suppression and (or) other side effects, weak efficacy of tumor treatment and even threatening patients’ life. How to enhance the killing effect of ROS on tumor cells while avoiding oxidative damage to the normal cells has become an urgent issue. This study is a review of the latest progress in the role of ROS-mediated programmed death in tumor treatment and prevention and treatment of oxidative damage in bone marrow induced by ROS.

Effect of Annexins Translocated in Extracellular Vesicles on Tumorigenesis

2020 ◽  
Vol 20 ◽  
Author(s):  
Qionghui Wu ◽  
Haidong Wei ◽  
Wenbo Meng ◽  
Xiaodong Xie ◽  
Zhenchang Zhang ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Extracellular Vesicles ◽  
Immune Cell ◽  
Epithelial Mesenchymal Transition ◽  
Main Role ◽  
Tumor Cell Adhesion ◽  
Mesenchymal Transition ◽  
Calcium Dependent ◽  
Tumor Neovascularization

: Annexin, a calcium-dependent phospholipid binding protein, can affect tumor cell adhesion, proliferation, apoptosis, invasion and metastasis, as well as tumor neovascularization in different ways. Recent studies have shown that annexin exists not only as an intracellular protein in tumor cells, but also in different ways to be secret outside the cell as a “crosstalk” tool for tumor cells and tumor microenvironment, thus playing an important role in the development of tumors, such as participating in epithelial-mesenchymal transition, regulating immune cell behavior, promoting neovascularization and so on. The mechanism of annexin secretion in the form of extracellular vesicles and its specific role is still unclear. This paper summarizes the main role of annexin secreted into the extracellular space in the form of extracellular vesicles in tumorigenesis and drug resistance and analyzes its possible mechanism.

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