scholarly journals Antibody-dependent cell-mediated cytotoxicity in the Moloney sarcoma virus system: differential activity of IgG and IgM with different subpopulations of lymphocytes.

1977 ◽  
Vol 145 (2) ◽  
pp. 302-313 ◽  
Author(s):  
E W Lamon ◽  
M W Shaw ◽  
S Goodson ◽  
B Lidin ◽  
A S Walia ◽  
...  
Keyword(s):  
Lymph Node ◽  
Target Cells ◽  
Effector Cells ◽  
Cortisone Injection ◽  
Sarcoma Virus ◽  
Dependent Cell ◽  
Lymph Node Cells ◽  
Moloney Sarcoma Virus ◽  
Differential Ability ◽  
Virus System

Antibody-dependent cell-mediated cytotoxicity in the Moloney sarcoma virus (MSV) system was evaluated in terms of the differential ability of IgG and IgM from MSV regressor animals to induce cytotoxicity by lymphocytes from lymph node, spleen, and thymus. The cell-mediated cytotoxicity induced by both IgM and IgG was specific for target possessing the appropriate virally determined cell surface antigen(s). IgM induced cytotoxicity by lymphocytes from all the organs tested. However, differences in magnitude and efficiency were revealed. Lymph node cells and thymocytes were most efficient against IgM-coated target cells. Against IgG-sensitized target cells, spleen and lymph node cells were about equally active, but thymocytes were inactive. Cortisone treatment of the donors of effector cells revealed that the cortisone resistant subpopulation of thymocytes, 2 days after cortisone injection, exhibited an increased cytotoxicity against target cells treated with unfractionated antiserum and its IgM fraction. This subpopulation of thymocytes was also cytotoxic against IgG-coated target cells. At 12 days after cortisone injection, the repopulated thymus showed little change in activity, compared to control thymus, against antibody-coated target cells.

Antibody-dependent cell-mediated cytotoxicity in the Moloney sarcoma virus system: No requirement for exogenous C5

1979 ◽  
Vol 14 (1) ◽  
pp. 35-46 ◽  
Author(s):  
Ernest W. Fuson ◽  
Amrik S. Walia ◽  
Betty A. Cox ◽  
Eddie W. Lamon
Keyword(s):  
Sarcoma Virus ◽  
Dependent Cell ◽  
Moloney Sarcoma Virus ◽  
Virus System

scholarly journals CYTOTOXICITY MEDIATED BY SOLUBLE ANTIGEN AND LYMPHOCYTES IN DELAYED HYPERSENSITIVITY

1968 ◽  
Vol 128 (6) ◽  
pp. 1237-1254 ◽  
Author(s):  
Nancy H. Ruddle ◽  
Byron H. Waksman
Keyword(s):  
Lymph Node ◽  
Genetic Difference ◽  
Specific Antigen ◽  
Delayed Hypersensitivity ◽  
Target Cells ◽  
Soluble Antigen ◽  
Rat Embryo ◽  
Egg Albumin ◽  
Lymph Node Cells ◽  
Electronic Particle Counter

In the presence of specific antigen, lymph node cells from inbred rats with delayed hypersensitivity to tuberculoprotein, bovine gammaglobulin, and egg albumin produced progressive destruction of monolayers of rat embryo fibroblasts in tissue culture, first apparent at 48 hr and maximal at 72 hr. The effect was specific and did not depend on a genetic difference between the lymph node cells and target cells. It required antigen concentrations equal to or greater than 1.25 µg/ml and lymphocyte: target cell ratios of approximately 10 or 20:1. It could be evaluated both by a plaquing technique and by cell enumeration with an electronic particle counter.

scholarly journals Massive upregulation of the Fas ligand in lpr and gld mice: implications for Fas regulation and the graft-versus-host disease-like wasting syndrome.

1995 ◽  
Vol 181 (1) ◽  
pp. 393-398 ◽  
Author(s):  
J L Chu ◽  
P Ramos ◽  
A Rosendorff ◽  
J Nikolić-Zugić ◽  
E Lacy ◽  
...  
Keyword(s):  
T Cells ◽  
Lymph Node ◽  
Fas Ligand ◽  
Target Cells ◽  
Dependent Manner ◽  
Wasting Syndrome ◽  
Positive Target ◽  
Abnormal Cells ◽  
Lymph Node Cells ◽  
Fasl Mrna

Fas-deficient lpr and gld mice develop lymphadenopathy due to the accumulation of T cells with an unusual double negative (DN) (CD4-CD8-) phenotype. Previous studies have shown that these abnormal cells are capable of inducing redirected lysis of certain Fc receptor-positive target cells. Since the Fas ligand (FasL) has recently been shown to be partly responsible for T cell-mediated cytotoxicity, lymph node cells from lpr and gld mice were examined for the expression of FasL mRNA. Northern blot analysis revealed that lymph node cells obtained from lpr and gld mice had a striking increase in the level of expression of FasL mRNA predominantly due to expression in the DN T cells. Furthermore, lpr, but not gld lymph node cells killed the B cell line, A20, in a Fas-dependent manner. These findings indicate that Fas mutations result in a massive up-regulation of FasL which, most likely, results from repetitive exposure to (self) antigen. This phenomenon could explain the lpr-induced wasting syndrome observed when lpr bone marrow-derived cells are adoptively transferred to wild-type recipients.

scholarly journals Characterization of Lyt-2-, L3T4- class I-specific cytolytic clones in C3H-gld/gld mice. Implications for functions of accessory molecules and programmed development.

1987 ◽  
Vol 166 (4) ◽  
pp. 1026-1040 ◽  
Author(s):  
K Yui ◽  
Y Hashimoto ◽  
S Wadsworth ◽  
M I Greene
Keyword(s):  
T Cells ◽  
Lymph Node ◽  
Gene Activation ◽  
Class I ◽  
Target Cells ◽  
Antigen Specificity ◽  
Lymph Node Cells ◽  
Accessory Molecules ◽  
Alpha Beta

We report the first demonstration of Thy-1+, Lyt-2-, L3T4- MHC-specific CTL clones derived from the Lyt-2-, L3T4- subset of lymph node cells of C3H-gld/gld mice. These clones express alpha/beta heterodimeric TCRs on the cell surface and specifically recognize class I molecules on target cells. Lyt-2 and L3T4 molecules are therefore not essential for the induction, recognition, and killing of antigen-specific CTL. In addition, these studies suggest that antigen specificity development for class I structures may occur before Lyt-2 gene activation in the differentiation of T cells.

scholarly journals Monocyte-mediated antibody-dependent cell-mediated cytotoxicity: the role of the metabolic burst

Blood ◽  
1981 ◽  
Vol 58 (2) ◽  
pp. 293-299
Author(s):  
CA Koller ◽  
AF LoBuglio
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Target Cells ◽  
Oxygen Species ◽  
Hexose Monophosphate ◽  
Human Monocytes ◽  
Effector Cells ◽  
Hypoxic Conditions ◽  
Dependent Cell

Human monocytes respond to opsonized microorganisms with a “metabolic burst” composed of an increase in oxygen consumption, an increase in hexose monophosphate shunt (HMPS) activity, and the generation of reactive oxygen species (ROS). We investigated the role of the metabolic burst in antibody-dependent cell-mediated cytotoxicity (ADCC) by human monocytes toward anti-D coated erythrocyte target cells because recent studies suggested a role for oxygen-dependent bactericidal mechanisms in ADCC. In normal monocytes, we found that ADCC was nearly halved under hypoxic conditions. Several agents known to impair activation of the burst, such as vincristine, cation chelators, and a sulfhydryl reagent, all decreased cytotoxicity if added before initiation of contact between target and effector cells. Cytotoxicity was inhibited by 2-deoxyglucose but not fluoride, suggesting a nonglycolytic role for glucose in ADCC, perhaps in the HMPS pathway. Although these data suggested a role for the metabolic burst in ADCC, scavengers of ROS did not impair cytotoxicity, and monocytes from chronic granulomatous disease (CGD) patients who had a defective metabolic burst had normal levels of ADCC. We conclude that ADCC toward anti-D coated erythrocyte target cells was the result of at least two independent but closely related cytotoxic pathways. Although one of these pathways appeared to involve the metabolic burst, the potentially cytotoxic reactive oxygen species did not appear to play a role in this system.

scholarly journals THE LYMPHOCYTE RESPONSE TO PRIMARY MOLONEY SARCOMA VIRUS TUMORS IN BALB/c MICE

1973 ◽  
Vol 137 (6) ◽  
pp. 1472-1493 ◽  
Author(s):  
E. W. Lamon ◽  
H. Wigzell ◽  
E. Klein ◽  
B. Andersson ◽  
H. M. Skurzak
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cell ◽  
Iron Powder ◽  
Cell Activity ◽  
Tumor Development ◽  
Cell Subpopulation ◽  
Target Cells ◽  
Sarcoma Virus ◽  
Moloney Sarcoma Virus

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.

scholarly journals Monocyte-mediated antibody-dependent cell-mediated cytotoxicity: the role of the metabolic burst

Blood ◽  
1981 ◽  
Vol 58 (2) ◽  
pp. 293-299 ◽  
Author(s):  
CA Koller ◽  
AF LoBuglio
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Target Cells ◽  
Oxygen Species ◽  
Hexose Monophosphate ◽  
Human Monocytes ◽  
Effector Cells ◽  
Hypoxic Conditions ◽  
Dependent Cell

Abstract Human monocytes respond to opsonized microorganisms with a “metabolic burst” composed of an increase in oxygen consumption, an increase in hexose monophosphate shunt (HMPS) activity, and the generation of reactive oxygen species (ROS). We investigated the role of the metabolic burst in antibody-dependent cell-mediated cytotoxicity (ADCC) by human monocytes toward anti-D coated erythrocyte target cells because recent studies suggested a role for oxygen-dependent bactericidal mechanisms in ADCC. In normal monocytes, we found that ADCC was nearly halved under hypoxic conditions. Several agents known to impair activation of the burst, such as vincristine, cation chelators, and a sulfhydryl reagent, all decreased cytotoxicity if added before initiation of contact between target and effector cells. Cytotoxicity was inhibited by 2-deoxyglucose but not fluoride, suggesting a nonglycolytic role for glucose in ADCC, perhaps in the HMPS pathway. Although these data suggested a role for the metabolic burst in ADCC, scavengers of ROS did not impair cytotoxicity, and monocytes from chronic granulomatous disease (CGD) patients who had a defective metabolic burst had normal levels of ADCC. We conclude that ADCC toward anti-D coated erythrocyte target cells was the result of at least two independent but closely related cytotoxic pathways. Although one of these pathways appeared to involve the metabolic burst, the potentially cytotoxic reactive oxygen species did not appear to play a role in this system.

scholarly journals H-2 antigens of the thymus determinelymphocyte specificity

1978 ◽  
Vol 148 (3) ◽  
pp. 766-775 ◽  
Author(s):  
PJ Fink ◽  
MJ Bevan
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Activity ◽  
Cytotoxic T Cell ◽  
Target Cells ◽  
Effector Cells ◽  
Minor Histocompatibility Antigens ◽  
Lymph Node Cells ◽  
Two Populations ◽  
Better Than

After immunization, normal H-2 heterozygous mice (for example H-2(b) × H-2(d)) generate two populations of cytotoxic effector T cells, one specific for target cells expressing H-2(b)-plus-antigen and the other specific for H- 2(d)-plus-antigen. With a multideterminant antigen, these two populations have about the same activity. We show here that the H-2 type of resident cells in the thymus determines the H-2 preference of cytotoxic T lymphocytes. F(1)(B 10 × B 10.D2) (H-2(b) × H-2 (d)) mice were thymectomized, lethally irradiated, and reconstituted with T-cell-depleted syngeneic hematopoietic cells. Groups of such ATXBM mice were grafted subcutaneously with neonatal thymus lobes from parental mice, either B10 (H-2 (b)) or B10.D2 (H-2(d)). 2-3 mo later, the mice were immunized against the minor histocompatibility antigens on F(1)(BALB/c × BALB.B) cells and assayed for cytotoxic T-cell activity. H-2(b) × H-2(d) ATXBM mice with H-2(b) thymus grafts responded to antigen-plus-H-2(b) much better than to antigen-plus-H-2(d), and vice versa for the mice with H-2(d) thymus grafts. As judged by antiserum treatment, the effector cells were of F(1) origin. To explore the possibility that the "thymus preference" may have been due to suppression of T-cell activity, nonimmune spleen and lymph node cells from normal H-2(b) × H-2(d) mice and cells from H-2(b) × H-2(d) mice bearing a homozygous thymus were mixed 1:1 and immunized in adoptive transfer. The mixture responded to antigen-plus-H-2(b) and antigen-plus-H-2(d) equally well, demonstrating that the cells that showed a "thymus preference" could not suppress a response to antigen in association with the nonthymic H-2 type. We conclude from these and other experiments that H-2 antigens present on resident cells of the thymus determine the spectrum of specificity of T cells which mature in that thymus and eventually make up the peripheral T- cell pool.

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