Failure of long surviving, passively enhanced kidney allografts to provoke T-dependent alloimmunity. II. Retransplantation of (AS X AUG)F1 kidneys from AS primary recipients into (AS X WF)F1 secondary hosts.
Long surviving, passively enhanced (AS X AUG)F1 kidneys carried by AS recipients were retransplanted into (AS X WF)F1 second hosts. Acute graft rejection did not occur. Only one of six secondary recipients mounted a significant T-dependent IgG lymphocytotoxic antibody response. In all six, generation of cytotoxic T cells was markedly slower and depressed. These results are compatible with the hypothesis that kidney parenchyma, although carrying major histocompatibility complex specificity is able to induce T-independent but not T-dependent alloimmunity. A corollary is that passenger cells are responsible for exciting the T-dependent allimmune response normally observed after grafing. The practical difficulty of eliminating all T-dependent immunogenicity from (AS X AUG)F1 kidneys was emphasized by the observation that a 3-d residence in an intermediate AS recipient was insufficient time to prevent acute graft rejection after retransplantation.
D000818:Animals; D006085:Graft Survival; D007111:Immunity, Cellular; D007116:Immunization, Passive; D007075:Immunoglobulin M / Q000096:biosynthesis; D007518:Isoantibodies / Q000096:biosynthesis*; D016030:Kidney Transplantation; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013601:T-Lymphocytes / Q000276:immunology*; D014184:Transplantation, Homologous
D007075:Immunoglobulin M; D007518:Isoantibodies