Anti-Friend virus antibody-induced resistance of Friend virus-infected spleen cells to lysis mediated by anti-H-2 antisera.

Possibleassociationshave been soughtbetween cell surface Friend murine erythroleukemia virus (FV)-en codedmoleculesandH-2 moleculesby subjectingspleen cells from infected mice to antibody-inducedcappingof one moleculeand then examiningthe cells for cocapping of the second.Cappingwas detectedbythe resistanceof capped cells to lysis by the capping antiserum and com plement. Three strains of mice congenicwith respect to the H-2 complexwere usedas sourcesof infectedspleen cells: BALB/c (H@2d),BALB.B (H-2'), and BALB.K (H@2k). Followingtreatment with anti-FV antiserumproducedby immunizationwithwhole virus,cells frommice of each of the three H-2 types demonstrateda drastic lossof sensi tivfty to anti-FV-mediated lysis, a partial but marked de crease in sensitivityto anti-H-2D-mediatedlysis, and an unalteredsusceptibilityto anti-H-2K-mediatedlysis,com pared to controlcells pretreatedwith normal mouse se rum. In the case of cells fromBALB.Kmice,cappingof FV antigenswith an anti-FV antiserumproducedin BALB.B mice againstsyngeneicFV-infectedtumorcells caused a decrease in sensitivityto 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 cocappingof H2Dd, H-2D'@, H@2Dk, and H@2Kkantigens with FV antigens is taken as evidence for a selective physical association between these molecules on infected cell surfaces.