Correlation of fetal kidney and testis congenic graft survival with reduced major histocompatibility complex burden

Prolonged survival was enjoyed by fetal and postnatal testis and midgestational renal grafts transplanted beneath the renal capsule of adult congenic mice, confirming previous findings in nonimmunosuppressed outbred rats (3, 5). The strategies that enable immature tissues to escape rejection in a graft survival assay were studied by comparing expression of major histocompatibility class I and class II protein and messenger ribonucleic acid (mRNA) in each tissue at different ages. In general, graft survival was best when class I and II expression was low. After transplantation, surviving kidney and testis grafts both showed marked induction of class I and II mRNA measured using donor and recipient—specific oligonucleotide probes. Immunohistochemically detected protein of both classes, however, could not be found in the kidney and was minimal in the testis. Fetal tissues appear to express lower levels of protein and mRNA— and, although invading lymphocytes may induce expression of class I and II mRNA after transplantation, protein was not inducible. The failure of these tissues to express significant levels of transplantation antigens may explain the prolonged survival of these immature grafts.