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Status of autoimmune diabetes 20-year after generation of bdc2.5-TCR transgenic non-obese diabetic mouse

World Journal of Diabetes 2013年第4期4卷 88-91页

作者： Lourdes Ramirez Abdel Rahim A Hamad Department of Pathology Johns Hopkins University School of Medicine

Type 1 diabetes(T1D) is an autoimmune disease that results from the destruction of insulin-producing cells by autoreactive T cells,leading to lifelong dependency on insulin therapy and increased risk of long-term cardiovascular *** we take the opportunity of the 20thanniversary of the generation of the bdc2.5 TCR transgenic non-obese diabetic(NOD) mouse model,to provide a brief overview of the significant progress that has been made in understanding the role of T cells in the disease pathogenesis *** included development of hundreds of reagents that block or even reverse new-onset disease by directly or indirectly controlling T *** also reflect on the sobering fact that none of these strategies has shown significant efficacy in clinical trials and discuss potential reasons hindering translation of the preclinical findings into successful therapeutic strategies and potential ways forward.

关键词： Autoimmune diabetes Immunotherapy T cells bdc2.5 T cells Anti-CD3 Immunosuppression

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I L- 15 trans-presentation regulates homeostasis of CD4^＋ T lymphocytes

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Cellular & Molecular Immunology 2014年第4期11卷 387-395页

作者： Xi-Lin Chen Diwakar Bobbala Yuneivy Cepero Donates Marian Mayhue Subburaj Ilangumaran Sheela Ramanathan Department of Pediatrics Immunology Division Faculty of Medicine and Health Sciences Universite de Sherbrooke Sherbrooke Que Canada Centre de recherche clinique Etienne-Le Bel Sherbrooke QC Canada

Interleukin-15 （IL-15） is essential for the survival of memory CD8^＋ and CD4^＋ T cell subsets, and natural killer and natural killer T cells. Here, we describe a hitherto unreported role of IL-15 in regulating homoeostasis of naive CD4^＋ T cells. Adoptive transfer of splenocytes from non-obese diabetic （NOD） mice results in increased homeostatic expansion of T cells in lymphopenic ***15^-/- mice when compared to *** recipients. The increased accumulation of CD4^＋ T cells is also observed in ***15^-/- mice, indicating that IL-15-dependent regulation also occurs in the absence of lymphopenia. *** mice lacking the I L- 15Ra chain, but not those lacking the common gamma chain, also show increased accumulation of CD4^＋ T cells. These findings indicate that the IL-15-mediated regulation occurs directly on CD4^＋ T cells and requires trans-presentation of IL-15. CD4^＋ T cells expanding in the absence of IL-15 signaling do not acquire the characteristics of classical regulatory T cells. Rather, CD4^＋ T cells expanding in the absence of IL-15 show impaired antigen-induced activation and IFN-7 production. Based on these findings, we propose that the IL-15-dependent regulation of the naive CD4^＋ T-cell compartment may represent an additional layer of control to thwart potentially autoreactive cells that escape central tolerance, while permitting the expansion of memory T cells.

关键词： bdc2.5 CD4^+ T cells homeostasis IL-15 NOD mouse

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