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Previous Volume 335:888-890 September 19, 1996 Number 12 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Given the autoimmune cause of insulin-dependent diabetes mellitus,¹ the theoretical barriers to successful pancreatic and islet transplantation are autoimmunity (destruction of beta cells due to recurrent autoimmunity) and alloimmunity (rejection of transplanted tissue from a genetically different person).² In this issue of the Journal, Tydén and coworkers provide evidence of the selective loss of beta cells in two patients with insulin-dependent diabetes mellitus in whom pancreatic allografts were rejected.³ Selective loss of the insulin-producing beta cells is the hallmark of autoimmune diabetes,⁴ and the islet cells that produce glucagon, somatostatin, and pancreatic polypeptide are spared. Beta-cell loss in allografts raises . . . [Full Text of this Article]

References

This article has been cited by other articles:

• Friedrichsen, B. N, Neubauer, N., Lee, Y. C, Gram, V. K, Blume, N., Petersen, J. S, Nielsen, J. H, Moldrup, A. (2006). Stimulation of pancreatic {beta}-cell replication by incretins involves transcriptional induction of cyclin D1 via multiple signalling pathways.. J Endocrinol 188: 481-492 [Abstract] [Full Text]  
• Slover, R. H., Eisenbarth, G. S. (1997). Prevention of Type I Diabetes and Recurrent {beta}-Cell Destruction of Transplanted Islets. Endocr. Rev. 18: 241-258 [Abstract] [Full Text]