Binding of monoclonal antibodies and T cell effector function in vivo.
The capacity of adoptively transferred CD8+ effector T cells to induce meningitis in immunosuppressed, or unsuppressed, recipients infected with lymphocytic choriomeningitis virus (LCMV) may be diminished by prior incubation of the lymphocytes with IgM monoclonal antibodies (MAbs) specific for CD8 or Thy1.2. The same is true, though to a lesser extent, for the further proliferation of donor T cells in the spleens of the immunosuppressed mice. This inhibition of cell mediated immunity can be overcome, at least for the unsuppressed recipients, by increasing the numbers of cells that are transferred, even though exposure to Mab+ complement abrogates all cytotoxic T cell activity in vitro. The LCM model thus provides a quantitative system for assessing the consequences of MAb binding for T cell trafficking and effector function in vivo.
Allan
J E
JE
John Curtin School of Medical Research, Canberra, Australia.
Doherty
P C
PC
D000818:Animals; D000911:Antibodies, Monoclonal / Q000378:metabolism*; D000945:Antigens, Differentiation, T-Lymphocyte; D000961:Antilymphocyte Serum / Q000378:metabolism; D016827:CD8 Antigens; D003520:Cyclophosphamide / Q000494:pharmacology; D007116:Immunization, Passive; D007165:Immunosuppression Therapy; D008216:Lymphocytic Choriomeningitis / Q000209:etiology; D051379:Mice; D008815:Mice, Inbred Strains; D013601:T-Lymphocytes / Q000276:immunology*; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology
D000911:Antibodies, Monoclonal; D000945:Antigens, Differentiation, T-Lymphocyte; D000961:Antilymphocyte Serum; D016827:CD8 Antigens; D003520:Cyclophosphamide