By Eleazar Shafrir
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Extra resources for Animal Models of Diabetes: Frontiers in Research, 2nd edition
J Biol Chem 278:54–63. Mackay IR, Bone A, Tuomi T, et al. (1996) Lack of autoimmune serological reactions in rodent models of insulin dependent diabetes mellitus. J Autoimmunity 9:705–711. MacMurray AJ, Moralejo DH, Kwitek AE, et al. (2002) Lymphopenia in the BB rat model of T1D is due to a mutation in a novel immune-associated nucleotide (lan)-related gene. Genome Res 12:1029–1039. Mahon JL, Dupre J, Stiller CR. (1993) Lessons learned from use of cyclosporine for insulindependent diabetes mellitus: The case for immunotherapy for insulin-dependent diabetics having residual insulin secretion.
Expl Clin Immunogenet 7:162–169. Geenen V, Brilot F. (2003) Role of the thymus in the development of tolerance and autoimmunity towards the neuroendocrine system. Ann NY Acad Sci 992:186–195. Georgiou HM, Bellgrau D. (1989) Thymus transplantation and disease prevention in the diabetes-prone BioBreeding rat. J Immunol 142:3400-3405. Georgiou HM, Lagarde AC, Bellgrau D. (1988) T cell dysfunction in the diabetes-prone BB rat. A role for thymic migrants that are not T cell precursors. J Exp Med 167:132–148.
Treg Depletion As noted earlier, spontaneous diabetes in lymphopenic BBDP/Wor rats can be prevented by transfusion with CD4+ART2+ Treg cells. Conversely, BBDR/Wor rats housed in conventional, non-VAF conditions become diabetic if treated with a depleting anti-ART2+ antibody (Greiner et al. 1987). Cyclophosphamide (Like et al. 1985) and low-dose irradiation (Handler et al. 1989) can also precipitate diabetes in this animal under these conditions, but whether the mechanism involves Treg populations is unknown.