scholarly journals SYNERGISTIC OR ANTAGONISTIC EFFECT OF DIFFERENT ANTIBODY CONCENTRATIONS ON IN VITRO LYMPHOCYTE CYTOTOXICITY IN THE MOLONEY SARCOMA VIRUS SYSTEM

1972 ◽  
Vol 135 (4) ◽  
pp. 997-1002 ◽  
Author(s):  
Henryk M. Skurzak ◽  
Eva Klein ◽  
Takato O. Yoshida ◽  
Eddie W. Lamon
1977 ◽  
Vol 145 (2) ◽  
pp. 302-313 ◽  
Author(s):  
E W Lamon ◽  
M W Shaw ◽  
S Goodson ◽  
B Lidin ◽  
A S Walia ◽  
...  

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.


Cell ◽  
1979 ◽  
Vol 16 (1) ◽  
pp. 63-75 ◽  
Author(s):  
Poul Andersson ◽  
Mitchell P. Goldfarb ◽  
Robert A. Weinberg

1983 ◽  
Vol 3 (3) ◽  
pp. 305-314
Author(s):  
M L McGeady ◽  
C Jhappan ◽  
R Ascione ◽  
G F Vande Woude

The transforming activity of cloned Moloney sarcoma virus (MSV) proviral DNA was inhibited by in vitro methylation of the DNA at cytosine residues, using HpaII and HhaI methylases before transfection into NIH 3T3 cells. The inhibition of transforming activity due to HpaII methylation was reversed by treatment of the transfected cells with 5-azacytidine, a specific inhibitor of methylation. Analysis of the genomic DNA from the transformed cells which resulted from the transfection of methylated MSV DNA revealed that the integrated MSV proviral DNA was sensitive to HpaII digestion in all cell lines examined, suggesting that loss of methyl groups was necessary for transformation. When cells were infected with Moloney murine leukemia virus at various times after transfection with methylated MSV DNA, the amount of transforming virus produced indicated that the loss of methyl groups occurred within 24 h. Methylation of MSV DNA at HhaI sites was as inhibitory to transforming activity as methylation at HpaII sites. In addition, methylation at both HpaII and HhaI sites did not further reduce the transforming activity of the DNA. These results suggested that; whereas methylation of specific sites on the provirus may not be essential for inhibiting the transforming activity of MSV DNA, methylation of specific regions may be necessary. Thus, by cotransfection of plasmids containing only specific regions of the MSV provirus, it was determined that methylation of the v-mos gene was more inhibitory to transformation than methylation of the viral long terminal repeat.


1979 ◽  
Vol 14 (1) ◽  
pp. 35-46 ◽  
Author(s):  
Ernest W. Fuson ◽  
Amrik S. Walia ◽  
Betty A. Cox ◽  
Eddie W. Lamon

1974 ◽  
Vol 13 (1) ◽  
pp. 32-40 ◽  
Author(s):  
H. Kirchner ◽  
R.B. Herberman ◽  
M. Glaser ◽  
D.H. Lavrin

1983 ◽  
Vol 3 (3) ◽  
pp. 305-314 ◽  
Author(s):  
M L McGeady ◽  
C Jhappan ◽  
R Ascione ◽  
G F Vande Woude

The transforming activity of cloned Moloney sarcoma virus (MSV) proviral DNA was inhibited by in vitro methylation of the DNA at cytosine residues, using HpaII and HhaI methylases before transfection into NIH 3T3 cells. The inhibition of transforming activity due to HpaII methylation was reversed by treatment of the transfected cells with 5-azacytidine, a specific inhibitor of methylation. Analysis of the genomic DNA from the transformed cells which resulted from the transfection of methylated MSV DNA revealed that the integrated MSV proviral DNA was sensitive to HpaII digestion in all cell lines examined, suggesting that loss of methyl groups was necessary for transformation. When cells were infected with Moloney murine leukemia virus at various times after transfection with methylated MSV DNA, the amount of transforming virus produced indicated that the loss of methyl groups occurred within 24 h. Methylation of MSV DNA at HhaI sites was as inhibitory to transforming activity as methylation at HpaII sites. In addition, methylation at both HpaII and HhaI sites did not further reduce the transforming activity of the DNA. These results suggested that; whereas methylation of specific sites on the provirus may not be essential for inhibiting the transforming activity of MSV DNA, methylation of specific regions may be necessary. Thus, by cotransfection of plasmids containing only specific regions of the MSV provirus, it was determined that methylation of the v-mos gene was more inhibitory to transformation than methylation of the viral long terminal repeat.


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