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Transfusion of Apoptotic β-Cells Induces Immune Tolerance to β-Cell Antigens and Prevents Type 1 Diabetes in NOD Mice.
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- Author(s): Xia, Chang-Qing; Peng, Ruihua; Qiu, Yushi; Annamalai, Mani; Gordon, David; Clare-Salzler, Michael J.
- Source:
Diabetes; Aug2007, Vol. 56 Issue 8, p2116-2123, 8p, 6 Graphs- Subject Terms:
- Source:
- Additional Information
- Abstract: In vivo induction of β-cell apoptosis has been demonstrated to be effective in preventing type I diabetes in NOD mice. Based on the notion that steady-state cell apoptosis is associated with self-tolerance and the need for developing a more practical approach using apoptotic β-cells to prevent type 1 diabetes, the current study was designed to investigate apoptotic β-cells induced ex vivo in preventing type 1 diabetes. The NIT-1 cell line serves as a source of β-cells. Apoptotic NIT-1 cells were prepared by ultraviolet B (UVB) irradiation. Three weekly transfusions of UVB-irradiated NIT-1 cells (1 x 105/mouse) or PBS were used to determine whether transfusions of UVB-irradiated NIT-1 cells induce immune tolerance to β-cell antigens in vivo and prevent type 1 diabetes. The suppression of anti-β-cell antibodies, polarization of T-helper (Th) cells, and induction of regulatory T-cells by UVB-irradiated NIT-1 cell treatment were investigated. The transfusions of apoptotic NIT-1 cells suppress anti-β-cell antibody development and induce Th2 responses and interleukin-10-producing regulatory type 1 cells. Importantly, this treatment significantly delays and prevents the onset of diabetes when 10-week-old NOD mice are treated. Adoptive transfer of splenocytes from UVB-irradiated NIT-1 cell-treated mice prevents diabetes caused by simultaneously injected diabetogenic splenocytes in NOD-Rag-/- mice. Moreover, the proliferation of adoptively transferred carboxyfluorescein diacetate succinimidyl ester-labeled β-cell antigen-specific T-cell receptor-transgenic T-cells in UVB-irradiated NIT-1- cell treated mice is markedly suppressed. The transfusion of apoptotic β-cells effectively protects against type 1 diabetes in NOD mice by inducing immune tolerance to β-cell antigens. This approach has great potential for immune intervention for human type 1 diabetes. Diabetes 56:2116-2123, 2007 [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Diabetes is the property of American Diabetes Association and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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