Properties of mouse leukemia viruses. XIX. Effective antibody therapy of AKR leukemia occurs independently of virus neutralization and produces long-term changes in the virus status of the thymus.
Administration of high-titered goat anti-FLV gp71 IgG to AKR mice during a narrow neonatal therapy "window" suppresses the early development of MuLV infectious cell centers (ICC) in spleen, thymus, and bone marrow. By 4-5 weeks of age ICC appear in spleen and marrow cell populations, rapidly increasing to plateau levels within 2 weeks in the absence of viremia. The thymus of treated animals remains devoid of detectable ICC throughout the 4-month period of testing. This pattern of ICC suppression occurs independently of virus neutralization as shown by the inability of F(ab')2 preparations, which retained neutralizing activity, to prevent early establishment of ICC. Immune IgG significantly decreases, but does not eliminate gp71 expression in all tissues tested. In control animals, ICC reside within a minor subpopulation of cortical, thymic T cells, whereas peripheral (i.e., splenic) ICC are totally devoid of conventional T cell, B cell, and macrophage phenotypic markers. Although thymocytes appear to be a major target of this antibody therapy, T-cell reactivity is not compromised.
D000406:AKR murine leukemia virus / Q000276:immunology*; D000818:Animals; D000831:Animals, Newborn; D000914:Antibodies, Viral / Q000008:administration & dosage*; D005434:Flow Cytometry; D007074:Immunoglobulin G / Q000008:administration & dosage; D007167:Immunotherapy; D009052:Leukemia Virus, Murine / Q000276:immunology*; D007942:Leukemia, Experimental / Q000276:immunology / Q000382:microbiology / Q000628:therapy*; D008213:Lymphocyte Activation; D008214:Lymphocytes / Q000276:immunology; D051379:Mice; D008806:Mice, Inbred AKR; D008934:Mitogens
D000914:Antibodies, Viral; D007074:Immunoglobulin G; D008934:Mitogens