Reversal of diabetes in non-obese diabetic mice without spleen cell-derived β cell regeneration

被引:100
作者
Chong, AS
Shen, JK
Tao, J
Yin, DP
Kuznetsov, A
Hara, M
Philipson, LH
机构
[1] Univ Chicago, Dept Surg, Sect Transplantat, Chicago, IL 60637 USA
[2] Univ Chicago, Dept Med, Endocrinol Sect, Chicago, IL 60637 USA
[3] Univ Illinois, Dept Surg, Chicago, IL 60612 USA
关键词
D O I
10.1126/science.1123510
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Autoimmune destruction of beta cells is the predominant cause of type 1 diabetes mellitus (T1DM) in humans and is modeled in non-obese diabetic (NOD) mice. Many therapeutic interventions prevent the development of T1DM in NOD mice, but few can induce its reversal once established. Intervention with Freund's complete adjuvant, semi-allogeneic splenocytes, and temporary islet transplantation has been reported to cure NOD mice of established T1DM. Using the same approach, we report here that this treatment cured 32% of NOD mice of established diabetes (>340 milligrams per deciliter blood glucose), although beta cells in these mice were not derived from donor splenocytes.
引用
收藏
页码:1774 / 1775
页数:2
相关论文
共 10 条
[1]   Genetic background determines the size and structure of the endocrine pancreas [J].
Bock, T ;
Pakkenberg, B ;
Buschard, K .
DIABETES, 2005, 54 (01) :133-137
[2]   Regulatory T cell lineage specification by the forkhead transcription factor FoxP3 [J].
Fontenot, JD ;
Rasmussen, JP ;
Williams, LM ;
Dooley, JL ;
Farr, AG ;
Rudensky, AY .
IMMUNITY, 2005, 22 (03) :329-341
[3]   Transgenic mice with green fluorescent protein-labeled pancreatic β-cells [J].
Hara, M ;
Wang, XY ;
Kawamura, T ;
Bindokas, VP ;
Dizon, RF ;
Alcoser, SY ;
Magnuson, MA ;
Bell, GI .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2003, 284 (01) :E177-E183
[4]   Effect of prophylactic insulin treatment on the number of ER-MP23(+) macrophages in the pancreas of NOD mice. Is the prevention of diabetes based on beta-cell rest? [J].
Jansen, A ;
Rosmalen, JGM ;
HomoDelarche, F ;
Dardenne, R ;
Drexhage, HA .
JOURNAL OF AUTOIMMUNITY, 1996, 9 (03) :341-348
[5]   Islet regeneration during the reversal of autoimmune diabetes in NOD mice [J].
Kodama, S ;
Kühtreiber, W ;
Fujimura, S ;
Dale, EA ;
Faustman, DL .
SCIENCE, 2003, 302 (5648) :1223-1227
[6]   Long-term islet allograft survival in nonobese diabetic mice treated with tacrolimus, rapamycin, and anti-interleukin-2 antibody [J].
Molano, RD ;
Pileggi, A ;
Berney, T ;
Poggioli, R ;
Zahr, E ;
Oliver, R ;
Malek, TR ;
Ricordi, C ;
Inverardi, L .
TRANSPLANTATION, 2003, 75 (11) :1812-1819
[7]   Islet abnormalities associated with an early influx of dendritic cells and macrophages in NOD and NODscid mice [J].
Rosmalen, JGM ;
Homo-Delarche, F ;
Durant, S ;
Kap, M ;
Leenen, PJM ;
Drexhage, HA .
LABORATORY INVESTIGATION, 2000, 80 (05) :769-777
[8]   Challenges facing islet transplantation for the treatment of type 1 diabetes mellitus [J].
Rother, KI ;
Harlan, DM .
JOURNAL OF CLINICAL INVESTIGATION, 2004, 114 (07) :877-883
[9]   Reversal of established autoimmune diabetes by restoration of endogenous β cell function [J].
Ryu, S ;
Kodama, S ;
Ryu, K ;
Schoenfeld, DA ;
Faustman, DL .
JOURNAL OF CLINICAL INVESTIGATION, 2001, 108 (01) :63-72
[10]   Immunological reversal of autoimmune diabetes without hematopoietic replacement of β cells [J].
Suri, A ;
Calderon, B ;
Esparza, TJ ;
Frederick, K ;
Bittner, P ;
Unanue, ER .
SCIENCE, 2006, 311 (5768) :1778-1780