title: Antibody to mouse interferon alpha/beta abrogates resistance to the multiplication of Friend erythroleukemia cells in the livers of allogeneic mice.
abstract: Friend erythroleukemia cells (FLC) (H-2d) injected intravenously into adult syngeneic DBA/2 or allogeneic C57B1/6 (H-2b) or C3H (H-2k) mice lodge in the liver but only multiply in the liver of syngeneic mice. Our results indicated that endogenous IFN-alpha/beta was a crucial factor in preventing the multiplication of FLC in the liver of adult allogeneic mice. (a) Treatment of allogeneic adult C57B1/6 or C3H mice with polyclonal antibody to mouse IFN-alpha/beta (but not antibody to IFN-gamma) completely abrogated the resistance to the multiplication of FLC in the liver and 87% of tumor-injected, antibody-treated C57B1/6 mice died with extensive tumor involvement of the liver. In contrast, after intravenous inoculation FLC do not multiply at all (or very rarely) in the liver of adult C57B1/6 mice left untreated or treated with a variety of control globulins, and no deaths occurred. (b) 8 h after intravenous inoculation of FLC, poly(A)+ RNA hybridizable with specific DNA probes for mouse IFN-alpha or -beta (but not -gamma) was present in the liver of injected C57B1/6 mice. Using the expression of the Mx protein as an indicator of the presence of IFN-alpha/beta, we showed that Mx+ congenic C57B1/6 mice injected with FLC exhibited a marked increase in the expression of the Mx protein in the liver, spleen, kidney and lung, and this increase was blocked by treatment of mice with antibody to IFN-alpha/beta. The possibility that different host mechanisms are elicited depending on the site of tumor growth in allogeneic mice is discussed. IFN-alpha/beta appears to be of particular importance in determining the resistance of the liver to FLC in allogeneic mice.
authors.affiliation: Laboratory of Viral Oncology, Groupe de Laboratoires de l'Institut de Recherches, Scientifiques sur le Cancer, Villejuif, France.
authors.forename: I
authors.initials: I
authors.lastname: Gresser
authors.forename: C
authors.initials: C
authors.lastname: Maury
authors.forename: F
authors.initials: F
authors.lastname: Vignaux
authors.forename: O
authors.initials: O
authors.lastname: Haller
authors.forename: F
authors.initials: F
authors.lastname: Belardelli
authors.forename: M G
authors.initials: MG
authors.lastname: Tovey
mesh_terms: D000367:Age Factors; D000818:Animals; D000906:Antibodies / Q000276:immunology; D000911:Antibodies, Monoclonal / Q000276:immunology; D000998:Antiviral Agents / Q000235:genetics / Q000276:immunology; D015342:DNA Probes; D005622:Friend murine leukemia virus; D019204:GTP-Binding Proteins; D007370:Interferon Type I / Q000276:immunology*; D004915:Leukemia, Erythroblastic, Acute / Q000276:immunology* / Q000473:pathology; D008114:Liver Neoplasms, Experimental / Q000276:immunology* / Q000473:pathology; D008285:Major Histocompatibility Complex; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D008811:Mice, Inbred DBA; D064547:Myxovirus Resistance Proteins; D009368:Neoplasm Transplantation; D011506:Proteins / Q000235:genetics / Q000276:immunology; D012333:RNA, Messenger / Q000032:analysis; D012712:Serum Globulins / Q000276:immunology; D014407:Tumor Cells, Cultured
chemical_list: D000906:Antibodies; D000911:Antibodies, Monoclonal; D000998:Antiviral Agents; D015342:DNA Probes; D007370:Interferon Type I; C579070:Mx1 protein, mouse; D064547:Myxovirus Resistance Proteins; D011506:Proteins; D012333:RNA, Messenger; D012712:Serum Globulins; D019204:GTP-Binding Proteins