Enhancement of Erythrocytic Maturation of Friend Virus-Induced Leukemia Cells in vitro1

2015 ◽  
pp. 943-954 ◽  
Author(s):  
H. Sugano ◽  
M. furusawa ◽  
T. Kawaguchi ◽  
Y. Ikawa
Keyword(s):  
Leukemia Cells ◽  
Friend Virus

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.

Reduced maturation of friend virus in adhesive mutants of friend leukemia cells

1987 ◽  
Vol 92 (1-2) ◽  
pp. 151-164
Author(s):  
C. Amici ◽  
C. Oppi ◽  
G. Fiorucci ◽  
A. Battistini ◽  
W. Djaczenko ◽  
...  
Keyword(s):  
Leukemia Cells ◽  
Friend Virus ◽  
Friend Leukemia

scholarly journals Role of Natural Killer Cells in Resistance against Friend Retrovirus-Induced Leukemia

2001 ◽  
Vol 75 (7) ◽  
pp. 3152-3163 ◽  
Author(s):  
Norimasa Iwanami ◽  
Atsuko Niwa ◽  
Yasuhiro Yasutomi ◽  
Nobutada Tabata ◽  
Masaaki Miyazawa
Keyword(s):  
T Cells ◽  
Natural Killer Cells ◽  
Natural Killer ◽  
Killer Cell ◽  
Leukemia Cells ◽  
Friend Virus ◽  
Killer Cells ◽  
Effector Cells ◽  
Friend Retrovirus ◽  
Retrovirus Infection

ABSTRACT We have previously shown that immunization with a synthetic peptide that contains a single CD4+ T-cell epitope protects mice against immunosuppressive Friend retrovirus infection. Cells producing infectious Friend virus were rapidly eliminated from the spleens of mice that had been immunized with the single-epitope peptide. However, actual effector mechanisms induced through T-helper-cell responses after Friend virus inoculation were unknown. When cytotoxic effector cells detected in the early phase of Friend retrovirus infection were separated based on their expression of cell surface markers, those lacking CD4 and CD8 but expressing natural killer cell markers were found to constitute the majority of effector cells that lysed Friend virus-induced leukemia cells. Depletion of natural killer cells by injecting anti-asialo-ganglio-N-tetraosylceramide antibody did not affect the number of CD4+ or CD8+ T cells in the spleen, virus antigen-specific proliferative responses of CD4+ T cells, or cytotoxic activity against Friend virus-induced leukemia cells exerted by CD8+ effector cells. However, the same treatment markedly reduced the killing activity of CD4− CD8−effector cells and completely abolished the effect of peptide immunization. Although the above enhancement of natural killer cell activity in the early stage of Friend virus infection was also observed in mice given no peptide, these results have demonstrated the importance and requirement of natural killer cells in vaccine-induced resistance against the retroviral infection.

Differentiation of Friend Virus-induced Leukemia Cells

2015 ◽  
pp. 221-228
Author(s):  
Haruo Sugano ◽  
Tokuichi Kawaguchi ◽  
Mitsuru Furusawa ◽  
Yoji Ikawa
Keyword(s):  
Leukemia Cells ◽  
Friend Virus

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 Studies on the role of the host immune response in recovery from Friend virus leukemia. I. Antiviral and antileukemia cell antibodies.

1976 ◽  
Vol 143 (1) ◽  
pp. 73-84 ◽  
Author(s):  
B Chesebro ◽  
K Wehrly
Keyword(s):  
Immune Response ◽  
Humoral Immune Response ◽  
Neutralizing Antibodies ◽  
Passive Transfer ◽  
Leukemia Cells ◽  
Friend Virus ◽  
Humoral Immune ◽  
Virus Leukemia

The humoral immune response to Friend virus leukemia was studied in congenic F1 mice differing in their incidence of recovery from leukemia. Antiviral neutralizing antibodies rose in titer in vivo concurrently with disappearance of viremia and fall in spleen virus levels. Cytotoxic antileukemia cell antibodies also appeared at this time. Passive transfer of these antibodies could inactivate low numbers of leukemia cells in vivo; however, mice of both high and low recovery genotypes produced antibodies in equal titer and recovered from viral infection in spite of striking differences in recovery from leukemic splenomegaly. Mice lacking C57BL genes did not produce antibodies or recover from viremia except in rare instances. Recovery from splenomegaly was found to be influenced by three or more C57BL genes independent of the H-2 complex.

Ferritin-Conjugated Antibody for the Demonstration of Isoantigens on the Surface of Murine Cells

1968 ◽  
Vol 26 ◽  
pp. 48-49
Author(s):  
T. Aoki ◽  
J. Izard ◽  
U. Hämmerling ◽  
E. de Harven ◽  
L. J. Old
Keyword(s):  
Cell Surface ◽  
Gamma Globulin ◽  
Leukemia Cells ◽  
Labelling Technique ◽  
Direct Labelling ◽  
Labelling Method

Although a variety of viral and cellular antigens have been demonstrated by ferritin-labeled antibody, this technique has not been used to locate isoantigens on the surface of nucleated cells. The recognition of several systems of isoantigens on the surface of thymocytes, lymphocytes and leukemia cells of the mouse and the ease with which these cells can be obtained in free suspension led us to consider the ferritin-labelling method to determine the amount and location of these isoantigens on the cell surface. Because of the problems involved in the direct labelling of mouse gamma globulin by ferritin, we have chosen an indirect labelling technique (i.e. ferritin-conjugated rabbit anti mouse γG)to detect localization of mouse isoantibody.

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