Magombedze Gesham, Nduru Polite, Bhunu Claver P, Mushayabasa Steady
Department of Applied Mathematics, National University of Science and Technology, PO Box AC939 Ascot, Bulawayo, Zimbabwe.
Biosystems. 2010 Nov-Dec;102(2-3):88-98. doi: 10.1016/j.biosystems.2010.07.018. Epub 2010 Aug 11.
Type 1 diabetes is a disease characterized by progressive loss of β cell function due to an autoimmune reaction affecting the islets of Langerhans. Two types of T cells are involved in diabetes: turncoat auto-reactive T cells, or T cells gone bad, that kill the insulin-producing cells, and regulatory T cells that are unable to control the auto-reactive T cells. We formulate a mathematical model that incorporates the role of cytotoxic T cells and regulatory T cells in type 1 diabetes. This study shows that onset of type 1 diabetes is due to a collective, dynamical instability, rather than being caused by a single etiological factor. It is also a numbers game between regulatory T cells and auto-reactive T cells. The problem in the onset of this disease is that there are not enough of the regulatory cells that suppress the immune response against the body's insulin-producing pancreatic islet cells.
1型糖尿病是一种由于影响胰岛的自身免疫反应导致β细胞功能逐渐丧失的疾病。有两种T细胞参与糖尿病的发生：叛变的自身反应性T细胞，即变坏的T细胞，它们会杀死产生胰岛素的细胞；以及无法控制自身反应性T细胞的调节性T细胞。我们构建了一个数学模型，该模型纳入了细胞毒性T细胞和调节性T细胞在1型糖尿病中的作用。这项研究表明，1型糖尿病的发病是由于一种集体性的动态不稳定性，而不是由单一病因引起的。这也是调节性T细胞和自身反应性T细胞之间的数量博弈。这种疾病发病的问题在于，能够抑制针对人体产生胰岛素的胰岛细胞的免疫反应的调节性细胞数量不足。
