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Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
Published on: May 6, 2013
Staphylococcus enterotoxin B-induced T cells can efficaciously protect against type 1 diabetes in non-obese diabetic
Yelei Guo1, Lei Xia2, Shilun Zhang3
1Department of Immunology Institute of Basic Medicine, School of Life Sciences, Chinese PLA General Hospital, Beijing, 100853, China.
Type 1 diabetes (T1D), an autoimmune disease, can be protected against by natural killer T (NKT) cells. Several attempts demonstrate that NKT cells also can be produced by inducing with Staphylococcus enterotoxin B (SEB) in addition to its classical activated antigen α-galactosylceramide. Here, we examined a potential usage of SEB-induced T (SEB-T) cells for the treatment of T1D. We established the immunophenotypes of SEB-T cells via flow cytometry, and in consequence, enriched in CD8(+)NKT cells after SEB stimulated. A high level of transforming growth factor β (TGF-β), detected by RT-PCR and ELISA, was first observed to be expressed and secreted by these SEB-T cells. Mixed lymphocyte reactions indicated that SEB-T cells could not produce a response to mitogens and allogeneic lymphocyte, and can inhibit lymphocytes response to mitogens. In an animal model, our data indicated that infusion of SEB-T cells in non-obese diabetic mice was well tolerated and could ameliorate hyperglycemia and maintain the blood glucose nearly on normal level until sacrifice. Strikingly, infusion of SEB-T cells resulted in an increase in the serum TGF-β level. These data raise the possibility that SEB-T cells can protect against T1D, which is associated with NKT cells generated in these SEB-induced cells.
Type 1 diabetes (T1D), an autoimmune disease, can be protected against by natural killer T (NKT) cells. Several attempts demonstrate that NKT cells also can be produced by inducing with Staphylococcus enterotoxin B (SEB) in addition to its classical activated antigen α-galactosylceramide. Here, we examined a potential usage of SEB-induced T (SEB-T) cells for the treatment of T1D. We established the immunophenotypes of SEB-T cells via flow cytometry, and in consequence, enriched in CD8(+)NKT cells after SEB stimulated. A high level of transforming growth factor β (TGF-β), detected by RT-PCR and ELISA, was first observed to be expressed and secreted by these SEB-T cells. Mixed lymphocyte reactions indicated that SEB-T cells could not produce a response to mitogens and allogeneic lymphocyte, and can inhibit lymphocytes response to mitogens. In an animal model, our data indicated that infusion of SEB-T cells in non-obese diabetic mice was well tolerated and could ameliorate hyperglycemia and maintain the blood glucose nearly on normal level until sacrifice. Strikingly, infusion of SEB-T cells resulted in an increase in the serum TGF-β level. These data raise the possibility that SEB-T cells can protect against T1D, which is associated with NKT cells generated in these SEB-induced cells.
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