A rat model for induction of transplantation tolerance, by antithymocyte globuline (ATG) as sole immunosuppressive agent, was studied. Vascularized heart allografts were employed. The conditions for establishment of long-term surviving (LTS) grafts were investigated as well as some of the characteristics of the tolerant state. The tolerance-inducing effect of ATG was found to be reproducible and dose-dependent. Treatment before grafting was essential. Preimmunization of the recipient inhibited the tolerance induction, while thymectomy seemed to have the opposite effect. The differences in survival of second allografts, third party or syngeneic to the first, indicated a largely strain-specific tolerance that most probably was the result of a changed host reactivity and for its induction strictly depended on presence of the graft. There were microscopical signs of rejection in the LTS grafts, while almost no such changes could be found in second allografts from the same donor strain, transplanted to the LTS-bearing recipients.

Summary. The development of diabetic glomerulopathy in kidneys transplanted to diabetic patients was estimated in transplant biopsies and evaluated in relation to suspected clinical risk factors for diabetic nephropathy. Surgical biopsies were taken at baseline and at 24-36 months post-transplantation in 16 Type 1 (insulin-dependent) diabetic patients and 8 non-diabetic control subjects with a glomerular filtration rate more than 30 ml. min * at follow-up. Immunosuppressive therapy included cyclosporine in all but one case. Stereological methods were used to assess basement membrane thickness, volume fraction of mesangium per glomerulus, and volume fraction of matrix per mesangium. The volume fraction of interstitial tissue per cortex was estimated by light microscopy. After 2 years the basement membrane thickness had increased by 55 nm (SD 58 nm) in the diabetic group. This change was significantly different from that of 2 nm (SD 37 nm) in control subjects (p = 0.02). Mesangial volume fraction increased significantly by 0.04 (SD 0.03) in diabetic patients, and this change was significantly different from that of -0.01 (SD 0.04) in non-diabetic patients (p =0.009). No change was detectable in the matrix expressed as fraction of mesangial volume. An increase in interstitial volume fraction from baseline to 2 years was observed, but was significant only in the diabetic group (p = 0.04). The changes in structural parameters did not correlate with mean values during follow-up of glycated haemoglobin or estimated protein intake, nor was any pattern discernible in the relationship to graft tissue types. The observed increase in basement membrane thickness corresponds to that observed in native kidneys during the first years of diabetes, whereas an increase in mesangial volume fraction-using a different protocol-was not observed in the early phase of the natural development. Absence of correlation with the various risk factors may reflect an irrelevance of these variables within the current range, or their influence may be offset by stronger mechanisms in the transplant situation, and therefore does not appear in this relatively small series.

Intravenous administration of ductus thoracicus lymph with dimeric IgA antibodies against Escherichia coli 06 to lactating rat dams did not result in transfer of IgA antibodies into the milk, although the antibodies were detectable in serum 1 min after the administration and in bile 60 min later. After intravenous injection of serum from bile-duct-occluded (BDO) rats immunized in the Peyer's patches into lactating rat dams. IgA antibodies appeared in the serum and remained there up to 230 min. At this time no IgA antibodies were seen in the milk while they were present in bile. IgG and IgM 06 antibodies did not appear in bile or milk after intravenous administration of lymph or serum from BDO rats.

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