Natural resistance to parental T-lymphocyte-induced immunosuppression in F1 hybrid mice: implications for acquired immune deficiency syndrome (AIDS).
The classical laws of transplantation which state that the major transplantation antigens are co-dominantly expressed do not account for the experimental observations that F1 hybrid mice can be genetically resistant to the growth of transplanted parental hemopoietic cells. Similarly, F1 mice can also be resistant to parental T-lymphocyte-induced immune suppression. The two phenomena are similar in that both: (a) mature relatively late in ontogeny; (b) can be over-ridden or saturated by excessive numbers of cells; and (c) the F1 host appears to recognize homozygous H-2Db of the donor. They differ in that many more cells appear to be required to over-ride resistance to immune suppression than to saturate resistance to bone-marrow grafts. The findings that natural resistance can be demonstrated for T-lymphocyte suppression of immune potential is discussed with respect to the synergistic effects of graft-versus-host disease and infection and the possible role of such resistance in susceptibility to acquired immune deficiency syndrome.
D000163:Acquired Immunodeficiency Syndrome / Q000276:immunology*; D000818:Animals; D006087:Graft vs Host Reaction; D006648:Histocompatibility; D006801:Humans; D006824:Hybridization, Genetic; D007108:Immune Tolerance; D007113:Immunity, Innate; D051379:Mice; D008815:Mice, Inbred Strains; D013601:T-Lymphocytes / Q000276:immunology* / Q000637:transplantation; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D014184:Transplantation, Homologous