Culture-derived neonatal Fisher-344 (Rt1(1v1)) rat islets have reduced immunogenicity and have been shown to be fully transplantable into Wistar Furth (Rtl(u)) recipicnts. In studies designed to test the MHC-restriction of the autoimmune disease process in the BB/Wor rat, MHC-matched (Wistar Furth) and MHC-mismatched (Fischer-344) nepnatal islets were isolated by a nonenzymatic tissue culture prpcedure and transplanted to the renal subcapsular site of BB/Wor rats before the onset of disease. All MHC-mismatched and most MHC-matched grafts survived intact. In this study we report the growth of MHC-matched and mismatched islet tissue at the graft site. Grafts in diabetes resistant animals averaged 60±26 μg, a comparable mass to that which was transplanted. Grafts in diabetic animals were significantly increased in size, averaging 176±156 μg (P=0.01). Analysis of nuclear to cytoplasmic volume ratios indicates that the increase in mass was primarily due to islet hyperplasia rather than hypertrophy. Factors contributing to the growth of islet tissue in situ are discussed.
|Original language||English (US)|
|Number of pages||6|
|Journal||Hormone and Metabolic Research|
|State||Published - 1990|