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Biochem Biophys Res Commun. 2008 Sep 19;374(2):282-7. doi: 10.1016/j.bbrc.2008.07.016. Epub 2008 Jul 14.

Reversal of new-onset type 1 diabetes in mice by syngeneic bone marrow transplantation.

Author information

1
Department of Hematology, The Affiliated Drum Tower Hospital of Nanjing University Medical School, 321, Zhongshan Road, Nanjing 210008, China.

Abstract

Autologous hematopoietic stem cell transplantation (HSCT) has recently been performed as a novel strategy to treat patients with new-onset type 1 diabetes (T1D). However, the mechanism of autologous HSCT-induced remission of diabetes remains unknown. In order to help clarify the mechanism of remission-induction following autologous HSCT in patients with T1D, mice treated with multiple low doses of streptozotocin to induce diabetes were used as both donors (n=20) and recipients (n=20). Compared to streptozocin-treated mice not receiving transplantation, syngeneic bone marrow transplantation (syn-BMT) from a streptozocin-treated diabetic donor, if applied during new-onset T1D (day 10 after diabetes onset), can reverse hyperglycemia without relapse (P<0.001), maintain normal blood insulin levels (P<0.001), and preserve islet cell mass. Compared to diabetic mice not undergoing HSCT, syn-BMT, results in restoration of Tregs in spleens (P<0.01), increased Foxp3 mRNA expression (P<0.01) and increased Foxp3 protein expression (P<0.05). This diabetic-remission-inducing effect occurred in mice receiving bone marrow from either streptozocin-treated diabetic or non-diabetic normal donors. We conclude that autologous HSCT remission of diabetes is more than transient immune suppression, and is capable of prolonged remission-induction via regeneration of CD4+CD25+FoxP3+ Tregs.

PMID:
18625200
DOI:
10.1016/j.bbrc.2008.07.016
[Indexed for MEDLINE]

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