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Department of Genetics, Albert Einstein College of Medicine, Bronx, New York 10461
Possible associations have been sought between cell surface Friend murine erythroleukemia virus (FV)-encoded molecules and H-2 molecules by subjecting spleen cells from infected mice to antibody-induced capping of one molecule and then examining the cells for cocapping of the second. Capping was detected by the resistance of capped cells to lysis by the capping antiserum and complement. Three strains of mice congenic with respect to the H-2 complex were used as sources of infected spleen cells: BALB/c (H-2d), BALB.B (H-2b), and BALB.K (H-2k). Following treatment with anti-FV antiserum produced by immunization with whole virus, cells from mice of each of the three H-2 types demonstrated a drastic loss of sensitivity to anti-FV-mediated lysis, a partial but marked decrease in sensitivity to anti-H-2D-mediated lysis, and an unaltered susceptibility to anti-H-2K-mediated lysis, compared to control cells pretreated with normal mouse serum. In the case of cells from BALB.K mice, capping of FV antigens with an anti-FV antiserum produced in BALB.B mice against syngeneic FV-infected tumor cells caused a decrease in sensitivity to anti-H-2Kk antiserum, as well as to anti-H-2Dk. In reciprocal experiments, capping with anti-H-2 sera did not cause a decrease in sensitivity to lysis by anti-FV antisera. The apparent cocapping of H-2Dd, H-2Db, H-2Dk, and H-2Kk antigens with FV antigens is taken as evidence for a selective physical association between these molecules on infected cell surfaces.
1 Supported by NIH Grant RO1 CA 19931 and Contract NO1 CP 71017.
2 Recipient of NIH Postdoctoral Fellowship F32 CA 09173. Present address: Department of Immunopathology, Scripps Clinic & Research Foundation, 10666 North Torrey Pines Road, La Jolla, Calif. 92037.
3 To whom requests for reprints should be addressed, at Department of Genetics, Albert Einstein College of Medicine, Bronx, N. Y. 10461.
Received 3/ 2/78. Accepted 5/30/78.
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