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12 March 1999

The Mechanism of Immunological "Enhancement" in Allografts- Distribution of Alloantigen and Alloantiserumin the Recipient

A Namyslowski, W L Olszewski

Ann Transplant 1999; 4(1): 31-38 :: ID: 497439


The active or passive "enhancement", by providing the recipient with donor cellular antigens and recipient antiserum against these antigens, has been known for long to prolong the survival time of organ allografts in rodents. Donor-specific blood transfusions seem to prolong the graft survival in animals and man evoking a similar protective mechanism. We investigated the mechanism of the effect of administering the recipient donor cells and antibodies against these cells on prolongation of heart graft survival. AUGust rat (RTIc) cells and WIStar rat (RTlu) antibodies against AUG antigens were labeled with 51 Cr and 1125, respectively. They were administered i.v. into prospective WIS recipients of AUG hearts -II and -10 days before grafting, respectively. The distribution and level of specific radioactivity were measured in the recipient lymphoid organs on days -9, -7 and -I as well as on days + I and +5 after transplantation. The highest levels of radioactivity of both donor cells and host antibodies against these cells were found on they -9 in recipient spleen but not liver, bone marrow and lymph nodes. After heart or skin transplantation. the radioactivity decreased in spleen to increase in liver and bone marrow. No specific accumulation of antibodies against donor antigens was detected in the grafts. These findings point to a role of antigen-antibody complexes located preferentially in the spleen on the downregulation of in vivo response to donor transplantation antigens. Aconcept of "continuous alloantigens elimination" is presented in which a systemic process of shed alloantigen inhibition and degradation in concert with blocking of organ surface antigens is presented.

Keywords: Enhancement, alloantibody, Transplantation

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Annals of Transplantation eISSN: 2329-0358
Annals of Transplantation eISSN: 2329-0358