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 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 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 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 New cell surface gp70 related to Friend mink cell focus-inducing virus is expressed on Friend virus-induced erythroleukemic spleen cells after elimination of ecotropic Friend virus gp70 in Rfv-3r/s mice.

1981 ◽  
Vol 154 (3) ◽  
pp. 868-882 ◽  
Author(s):  
W J Britt ◽  
J K Collins ◽  
B Chesebro
Keyword(s):  
Cell Surface ◽  
Leukemia Cell ◽  
Helper Virus ◽  
Leukemic Cells ◽  
Friend Virus ◽  
Spleen Cells ◽  
Virus Inoculation ◽  
Recombinant Viruses ◽  
Friend Virus Infection ◽  
Mink Cell

Spleen cells from Rfv-3r/s mice with Friend virus-induced erythroleukemia were analyzed for expression of virus-induced proteins with monoclonal antiviral antibodies and conventional antisera. Leukemic spleen cells, 30-60 d after virus inoculation, expressed decreased amounts of ecotropic Friend murine leukemia helper virus gag- and env-encoded cell surface and intracellular proteins compared with leukemic cells tested 8-10 d after virus inoculation. In contrast, the spleen focus-forming virus-induced protein, gp55, was present on both leukemia cell populations. This difference appeared to be mediated by the humoral antibody response in Rfv-3r/s mice, which could recognize only ecotropic gag and env proteins, and not gp55. A new gp70 molecule cross-reactive with a recombinant Friend mink cell focus-inducing virus was found in large quantities on late leukemic cells. This protein appeared to be derived from a recombinant virus produced during the course of Friend virus infection. The appearance of this new gp70 suggests that recombinant viruses other than spleen focus-forming virus may play a role in Friend virus-induced erythroleukemia.

scholarly journals Immunologic classification of lymphocytic leukemias based on monoclonal antibody-defined cell surface antigens

Blood ◽  
1982 ◽  
Vol 59 (2) ◽  
pp. 207-215
Author(s):  
RW Schroff ◽  
KA Foon ◽  
RJ Billing ◽  
JL Fahey
Keyword(s):  
Cell Surface ◽  
B Cell ◽  
Cell Lineage ◽  
Antigen Expression ◽  
Surface Antigens ◽  
Lymphocytic Leukemia ◽  
Leukemic Cells ◽  
Cell Surface Antigens ◽  
Prolymphocytic Leukemia ◽  
Hla Dr

A panel of monoclonal antibodies reactive with normal lymphocyte subsets was used to classify cases of lymphocytic leukemia on the basis of cell surface antigen expression. The antibodies employed were commercially available and included a common framework HLA-DR antibody, two pan-T antibodies (Leu-1 and OKT-3), and antibodies defining cytotoxic/suppressor (Leu-2 and OKT-8) and helper/inducer (Leu-3 and OKT-4) subpopulations of normal T lymphocytes. Cases of ALL could be subgrouped into non-T non-B, pre-T and T-ALL on the basis of reactivity with HLA-DR, Leu-1, and OKT-3 antibodies. Leukemic cells from patients with T-cell CLL could be divided into Leu-2/OKT-8 reactive and Leu- 3/OKT-4 reactive subpopulations, as well as a subgroup in which the majority of cells were unreactive with either of these antibodies. With the exception of one individual, all Sezary cell leukemias expressed a phenotypic pattern similar to that of the Leu-3 subgroup of T-CLL. Malignancies of B-cell lineage (B-CLL, prolymphocytic leukemia, and lymphosarcoma) that were examined were reactive with both the HLA-DR and Leu-1 antibodies. On the contrary, normal B lymphocytes and lymphoid cell lines of B-cell origin did not express surface antigens recognized by the Leu-1 antibody.

scholarly journals Immunologic classification of lymphocytic leukemias based on monoclonal antibody-defined cell surface antigens

Blood ◽  
1982 ◽  
Vol 59 (2) ◽  
pp. 207-215 ◽  
Author(s):  
RW Schroff ◽  
KA Foon ◽  
RJ Billing ◽  
JL Fahey
Keyword(s):  
Cell Surface ◽  
B Cell ◽  
Cell Lineage ◽  
Antigen Expression ◽  
Surface Antigens ◽  
Lymphocytic Leukemia ◽  
Leukemic Cells ◽  
Cell Surface Antigens ◽  
Prolymphocytic Leukemia ◽  
Hla Dr

Abstract A panel of monoclonal antibodies reactive with normal lymphocyte subsets was used to classify cases of lymphocytic leukemia on the basis of cell surface antigen expression. The antibodies employed were commercially available and included a common framework HLA-DR antibody, two pan-T antibodies (Leu-1 and OKT-3), and antibodies defining cytotoxic/suppressor (Leu-2 and OKT-8) and helper/inducer (Leu-3 and OKT-4) subpopulations of normal T lymphocytes. Cases of ALL could be subgrouped into non-T non-B, pre-T and T-ALL on the basis of reactivity with HLA-DR, Leu-1, and OKT-3 antibodies. Leukemic cells from patients with T-cell CLL could be divided into Leu-2/OKT-8 reactive and Leu- 3/OKT-4 reactive subpopulations, as well as a subgroup in which the majority of cells were unreactive with either of these antibodies. With the exception of one individual, all Sezary cell leukemias expressed a phenotypic pattern similar to that of the Leu-3 subgroup of T-CLL. Malignancies of B-cell lineage (B-CLL, prolymphocytic leukemia, and lymphosarcoma) that were examined were reactive with both the HLA-DR and Leu-1 antibodies. On the contrary, normal B lymphocytes and lymphoid cell lines of B-cell origin did not express surface antigens recognized by the Leu-1 antibody.

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