Examination of Serum Class I Antigen in Allograft Recipient Rats : Origin and control of serum class I antigen

We examined the appearance of DA type (RT1Aa) class I antigen in the serum of rats that had received isogeneic or allogeneic liver grafts (DA into DA, DA into LEW, PVG into DA, PVG into F1 hybrid (DAxPVG). Recipient LEW rats were given either one injection of the anti-CD8 mAb, OX-8, following thymectomy or anti-CD4 mAb (cocktail of OX-35 and OX-38) following thymectomy 3 days prior to liver grafting. We also tested the serum RT1Aa antigen titer of F1 (DAxPVG) recipients after PVG spleen transplantation and the serum RT1Aa antigen titer in the DA rat after hepatectomy and cyclosporin treatment.　　

Replacement of DA liver by PVG lowered transiently the serum level of RT1Aa antigen to 70% of that in normal DA serum, shortly after liver transplantation. However, this titer increased gradually over the level in normal DA serum.　　

A PVG spleen graft to an F1 hybrid recipient resulted in death due to typical GVH disease between 13 and 24 days after spleen transplantation. The RT1Aa antigen titer increased to several times more than that in normal F1 serum throughout the observation period.　　

LEW recipients of DA liver died at 9-11 days (9.8± 1.1 days) due to acute liver rejection. In this combination, the serum level of RT1Aa increased until day 8, reaching a maximum (four times) on day 4. Deletion of either CD8+ or CD4+ T cells by anti-CD8 or anti-CD4 MAb in this transplantation prolonged the survival times of liver grafts for up to 26.8±8.4 and 35.6± 17.9 days, respectively. In the anti-CD8 or anti-CD4 MAb- treated recipients, the serum titer of DA class I antigen was not elevated and there were no differences between the two. Hepatectomy in combination with cyclosporin induced a high titer of liver- derived class I antigen in the serum as long as liver regeneration proceeded.　　

These results suggest that the liver is the principal source of serum class I antigen in rats. Rejection, GVH reaction and liver regeneration increased the serum class I antigen from transplanted liver or host tissue. It is unlikely that this is due to cleavage of membranous class I antigen by class I- reactive CD8+ T cells.