Ptak W, Rewicka M, Kollat M
Nature. 1980 Jan 10;283(5743):199-200. doi: 10.1038/283199a0.
Mice and rats injected with alloxan or streptozotocin develop permanent diabetes, characterised by deficient insulin production. It has been demonstrated that hypoinsulinaemia in mice leads to significant loss of lymphatic tissue, and these diabetic animals cannot develop contact sensitivity or efficient graft rejection. Administration of insulin partially restored these responses and also caused an increase in the weight of the thymus and spleen. Similar suppression of T cell-dependent phenomena has been observed in surgically pancreatectomised rats. Lymphocytes of these hypoinsulinaemic animals show significantly decreased in vitro responses to plant lectins and generate only low levels of cytotoxic effector cells. We previously showed that cells of normoglycaemic oxazolone-sensitised mice cannot transfer significant contact sensitivity reactions into diabetic recipients indicating that the milieu of hyperglycaemic insulin deficient animals cannot support all the activity of immune T cells. By mixing immunised T cells from control and diabetic mice and transferring the mixtures into normal recipients we now show that the non-supportive millieu in diabetic animals may be due to active suppression rather than to athrepsis.
注射了四氧嘧啶或链脲佐菌素的小鼠和大鼠会患上永久性糖尿病，其特征是胰岛素分泌不足。已经证明，小鼠的低胰岛素血症会导致淋巴组织显著减少，并且这些糖尿病动物无法产生接触敏感性或有效的移植排斥反应。给予胰岛素可部分恢复这些反应，还会导致胸腺和脾脏重量增加。在接受手术切除胰腺的大鼠中也观察到了类似的对T细胞依赖性现象的抑制。这些低胰岛素血症动物的淋巴细胞对植物凝集素的体外反应显著降低，并且仅产生低水平的细胞毒性效应细胞。我们之前表明，血糖正常的恶唑酮致敏小鼠的细胞无法将显著的接触敏感性反应传递给糖尿病受体，这表明高血糖胰岛素缺乏动物的环境无法支持免疫T细胞的所有活性。通过将来自对照小鼠和糖尿病小鼠的免疫T细胞混合并将混合物转移到正常受体中，我们现在表明糖尿病动物中这种非支持性环境可能是由于主动抑制而非营养缺乏。
