[Immune status of indefinitely surviving rat renal allograft recipients after short course of ALS-treatment Detection of a serum blocking factor by allorosette formation inhibition test (author's transl)].
53 LBNF1 kidneys were grafted into L-rats. 24 untreated recipients served as control and survived 16.1 +/- 1.7 days. 14 recipients were treated with 4 ml alloantiserum (ADS) each, and the other 15 animals with 4 ml ALS each. 9 and 10 of these 14 and 15 animals survived for more than 4 months. We performed GvH-reaction with spleen cells of these 19 animals. It showed normal cellular immune response. After splenectomy first donor specific skin was transplanted, 18 days later second skin of same origin (LBNF1) and 18' days after third party skin (LBufF1). The first grafts survived 13.1 +/- 1.9 days in the recipients of ADS treatment and 12.2 +/- 1.2 days in the recipients of ALS. Second skin grafts were rejected delayed in the former recipients as the first grafts, in the later more accelerated than the first grafts. The third grafts survived as the controls. Before and after skin grafting we could not detect lymphocytotoxin and hemagglutinin. The sera of animals with ADS therapy inhibited the spontaneous allorosette formation to 46.0 +/- 4.4% and of ALS therapy 37.7 +/- 9.2%. Our results suggest that after ALS treatment blocking antibodies were produced in the recipients and they cause the enhancement of kidney allograft.
[Immune status of indefinitely surviving rat renal allograft recipients after short course of ALS-treatment Detection of a serum blocking factor by allorosette formation inhibition test (author's transl)]. 53 LBNF1 kidneys were grafted into L-rats. 24 untreated recipients served as control and survived 16.1 +/- 1.7 days. 14 recipients were treated with 4 ml alloantiserum (ADS) each, and the other 15 animals with 4 ml ALS each. 9 and 10 of these 14 and 15 animals survived for more than 4 months. We performed GvH-reaction with spleen cells of these 19 animals. It showed normal cellular immune response. After splenectomy first donor specific skin was transplanted, 18 days later second skin of same origin (LBNF1) and 18' days after third party skin (LBufF1). The first grafts survived 13.1 +/- 1.9 days in the recipients of ADS treatment and 12.2 +/- 1.2 days in the recipients of ALS. Second skin grafts were rejected delayed in the former recipients as the first grafts, in the later more accelerated than the first grafts. The third grafts survived as the controls. Before and after skin grafting we could not detect lymphocytotoxin and hemagglutinin. The sera of animals with ADS therapy inhibited the spontaneous allorosette formation to 46.0 +/- 4.4% and of ALS therapy 37.7 +/- 9.2%. Our results suggest that after ALS treatment blocking antibodies were produced in the recipients and they cause the enhancement of kidney allograft.