scholarly journals A NEW SENSITIVE ASSAY FOR ANTIBODY AGAINST CELL SURFACE ANTIGENS BASED ON INHIBITION OF CELL-DEPENDENT ANTIBODY-MEDIATED CYTOTOXICITY

1974 ◽  
Vol 140 (5) ◽  
pp. 1348-1363 ◽  
Author(s):  
Phil Halloran ◽  
Volker Schirrmacher ◽  
Hilliard Festenstein
Keyword(s):  
Cell Surface ◽  
Surface Antigens ◽  
Target Cells ◽  
Sensitive Assay ◽  
Spleen Cells ◽  
Antibody Assay ◽  
Cell Surface Antigens ◽  
Effector Cells ◽  
Cell Antibody ◽  
Chicken Erythrocytes

Inhibition of cell-dependent antibody-mediated cytotoxicity has been investigated as a new assay for antibody against cell surface antigens. The cytotoxicity system consisted of effector cells (normal mouse spleen cells), target cells (61Cr-labeled chicken erythrocytes), and antitarget cell antibody. Addition of antibody against cell surface antigens in the effector cell population regularly inhibited the cytotoxicity measured in this system. This cytotoxicity inhibition assay (CIA) detected antibody with a variety of specificities: anti-H-2, anti-Thy 1.2, anti-immunoglobulin, and antimouse bone marrow-derived lymphocyte antigen. When the inhibition by anti-H-2 sera was analyzed using effector cells from congenic mice, the activity was found to be directed against specificities mapping in the H-2K, H-2D, and I regions of the H-2 complex, correlating well with the specificities characterized by complement-dependent assays. A comparison between the sensitivity of the CIA and complement-dependent lysis revealed that the CIA was 2–11 times more sensitive for anti-H-2 antisera and 20–780 times more sensitive for certain antisera against subpopulations of the spleen cells (i.e., T cells or B cells). The CIA proved to be precise, sensitive, and reliable. It may become a very useful antibody assay in various species including man.

scholarly journals Genetic regulation of the antibody response to H-2Db alloantigens in mice. I. Differences in activation of helper T cells in C57BL/10 and BALB/c congenic strains.

1975 ◽  
Vol 141 (3) ◽  
pp. 573-583 ◽  
Author(s):  
D Wernet ◽  
F Lilly
Keyword(s):  
T Cell ◽  
Cell Surface ◽  
Antibody Response ◽  
Genetic Regulation ◽  
Surface Antigens ◽  
T Helper ◽  
Spleen Cells ◽  
Igg Antibody ◽  
Cell Surface Antigens ◽  
Helper Function

B10.A(5R) mice immunized with C57BL/10 spleen cells demonstrate a normal T-cell-mediated cytotoxicity to H-2Db tumor cells but they do not mount any IgG antibody response to H-2Db alloantigens. B10.A(5R) mice do show a high titered IgG response when immunized with A.BY cells, which differ at H-2Db plus non-H-2 cell surface antigens, or with B10.A(2R) cells, which differ at H-2Db, H-2Kk, and H-2Ik cell surface antigens. These findings indicate a failure of the T-helper cells to induce the switch from IgM to IgG when the H-2Db alloantigens are the only difference on the immunizing cell. In immunizing H-2d mice with congenic H-g2 cells which differ only in the H-2Db region, mice of the C57BL/10 background made only IgM antibodies whereas mice of the BALB/c background made IgG antibodies. This comparison confirms that genes separate from H-2 regulate the T-cell helper function. The genes that influence the T-cell helper function do not regulate the T-cell-mediated cytotoxicity.

scholarly journals Antibody-induced loss of Friend virus leukemia cell surface antigens occurs during progression of erythroleukemia in F1 mice.

1978 ◽  
Vol 148 (5) ◽  
pp. 1109-1121 ◽  
Author(s):  
D Doig ◽  
B Chesebro
Keyword(s):  
Cell Surface ◽  
Leukemia Cell ◽  
Surface Antigens ◽  
Leukemia Cells ◽  
Friend Virus ◽  
Spleen Cells ◽  
Cell Surface Antigens ◽  
Fv Antibody ◽  
Quantitative Absorption ◽  
Antigen Loss

Friend virus (FV)-induced leukemic spleen cells from (B10.A X A)F1 mice were found to lose sensitivity to antibody-mediated lysis during progression of erythroleukemia. This was correlated with a 78% loss of FV-induced cell surface antigens as determined by quantitative absorption of cytotoxic antibodies and with a decreased percentage of leukemic spleen cells showing membrane immunofluorescence with anti-FV antibody. Antigen loss was observed only with virus-induced antigens, and was limited to antigens expressed on the cell surface. FV-induced antigens were regained when low-antigen leukemia cells from late stages of the leukemia were transferred to lethally irradiated nonimmune recipients, but not when these cells were transferred to hyperimmune lethally irradiated recipients. Conversely, when high-antigen leukemic spleen cells from early stages of the erythroleukemia were transferred to hyperimmune irradiated recipients, antigen loss was induced. The immune response to virus-induced antigens appeared to be involved in causing the antigenic changes observed on leukemia cells in this system.

scholarly journals Localization of aggregated cell surface antigens of target cells bound to cytotoxic T lymphocytes.

1975 ◽  
Vol 142 (4) ◽  
pp. 1011-1016 ◽  
Author(s):  
G Berke ◽  
Z V Fishelson
Keyword(s):  
T Lymphocytes ◽  
Cell Surface ◽  
Cytotoxic T Lymphocytes ◽  
Target Cell ◽  
Cytotoxic T Lymphocyte ◽  
Surface Antigens ◽  
Cell Interaction ◽  
Target Cells ◽  
Cell Surface Antigens ◽  
Polar Localization

The redistribution of aggregated cell surface antigens of target cells bound to cytotoxic T lymphocytes was investigated. It was found that cap formation induced by antibody always occurred toward the site of binding. It is suggested that the polar localization of capped target cell surface determinants is a consequence of cytotoxic T-lymphocyte target cell interaction.

scholarly journals Anti-Friend virus antibody is associated with recovery from viremia and loss of viral leukemia cell-surface antigens in leukemic mice. Identification of Rfv-3 as a gene locus influencing antibody production.

1979 ◽  
Vol 150 (1) ◽  
pp. 10-19 ◽  
Author(s):  
D Doig ◽  
B Chesebro
Keyword(s):  
Cell Surface ◽  
Genetic Locus ◽  
Leukemia Cell ◽  
Antigen Expression ◽  
Surface Antigens ◽  
Leukemia Cells ◽  
Friend Virus ◽  
Spleen Cells ◽  
Cell Surface Antigens ◽  
Antigen Loss

A single genetic locus, Rfv-3, influenced Friend virus (FV) viremia, loss of FV-induced cell-surface antigens from leukemia cells, and generation of anti-FV antibodies. 30--90 d after FV infection leukemic spleen cells from (B10.A X A)F1 and (B10.A X A.BY)F1 mice (Rfv-3r/s) were found to have low FV-induced cell-surface antigen expression compared to leukemic spleen cells from A and A.BY mice (Rfv-3s/s). In addition, these F1 mice recovered from viremia and generated cytotoxic anti-FV antibodies. A and A.BY mice did not recover from viremia and failed to generate anti-FV antibodies. Anti-FV leukemia cell antibody appeared to mediate FV-antigen loss because decrease of FV cell-surface antigens occurred at the same time as anti-FV antibody appeared in the plasma of F1 mice, and passive transfer of anti-FV antisera induced modulation of FV cell-surface antigens. Rfv-3 did not influence an intrinsic ability of FV antigens to be modulated from Rfv-3s/s leukemia cells because FV antigen loss from Rfv-3s/s spleen cells occurred after transfer of cells to an immune environment.

scholarly journals Multiple activities of a cloned cell line mediating natural killer cell function.

1981 ◽  
Vol 153 (6) ◽  
pp. 1582-1591 ◽  
Author(s):  
G Nabel ◽  
L R Bucalo ◽  
J Allard ◽  
H Wigzell ◽  
H Cantor
Keyword(s):  
Cell Surface ◽  
Nk Cells ◽  
Natural Killer ◽  
Cell Line ◽  
Cell Function ◽  
Nk Cell ◽  
Killer Cell ◽  
Surface Antigens ◽  
Target Cells ◽  
Cell Surface Antigens

A special class of immunologic cells can lyse or damage a variety of target cells, notably malignant cells in vitro. These cells have been called natural killer (NK) cells because lysis does not require deliberate immunization by tumor cells. Although these cells can be distinguished from conventional T cells, B cells, and phagocytic cells, they have been difficult to define. We describe a representative cloned cell line that was obtained by cloning Ig -Ly-5+ cells from spleen. This clone, Cl.Ly-1-2-NK-1+/11, displays Thy-1, Ly-5, Qat-4, Qat-5 and NK-1 cell surface antigens and lyses the NK-sensitive YAC-1 lymphoma cells, but does not lyse RL-12 cells, an NK-resistant lymphoma. In addition, this clone lysed the P815 mastocytoma, EL4 lymphoma, and lipopolysaccharide-activated B lymphocyte targets. This cloned population therefore combined information for a unique display of cell surface antigens and specialized function similar to "activated" NK cells. Because this cloned population forms conjugates with susceptible but not resistant target cells, it may prove useful to identify the structure of cell surface molecules that recognize foreign cells. Finally, cells of this clone also specificity lysed target cells coated by antibodies to determinants on the target cell surface, demonstrating that a single cloned cell population can mediate two specialized immunologic functions: antibody-dependent cellular cytotoxicity and NK cell lysis.

scholarly journals Genetic regulation of the antibody response to H-2Db alloantigens in mice. II. Tolerance to non-H-2 determinants abolishes the antibody response to H-2Db in B10.A(5R) mice.

1976 ◽  
Vol 144 (1) ◽  
pp. 266-271 ◽  
Author(s):  
D Wernet ◽  
F Lilly
Keyword(s):  
T Cell ◽  
Cell Surface ◽  
Antibody Response ◽  
Genetic Regulation ◽  
Tolerance Induction ◽  
Surface Antigens ◽  
Igg Antibodies ◽  
Spleen Cells ◽  
Cell Surface Antigens ◽  
Helper Function

B10.A(5R) mice (H-2i5), immunized with spleen cells from congenic B10 mice (H-2b), responded to alloantigens of the H-2Db region by producing antibodies of only IgM type. In contrast, they produced both IgM and IgG antibodies when immunized with noncongenic H-2b cells that carry other foreign cell surface antigens (non-H-2) in addition to H-2Db. A hypothesis was proposed comparing the H-2Db antigen on a congenic cell to a hapten on a nonimmunogenic carrier which fails to induce T-cell helper function responsible for the switch from IgM to IgG secretion in B cells. Data presented here confirmed this hypothesis. 5R mice rendered tolerant to the relevant non-H-2 antigens were unable to mount the anti-H-2Db IgG response in a noncongenic immunization. Tolerance induction did not lead to abrogation of the T-cell mediated cytotoxicity.

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