Development of specific suppressor cells in hypoinsulinaemic mice

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Abstract
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 tissue1,2, and these diabetic animals cannot develop contact sensitivity1 or efficient graft rejection3,4. Administration of insulin partially restored these responses1,4 and also caused an increase in the weight of the thymus and spleen1. Similar suppression of T cell-dependent phenomena has been observed in surgically pancreatectomised rats5. Lymphocytes of these hypoinsulinaemic animals show significantly decreased in vitro responses to plant lectins2,6,7 and generate only low levels of cytotoxic effector cells2,7. We previously showed that cells of normoglycaemic oxazolone-sensitised mice cannot transfer significant contact sensitivity reactions into diabetic recipients1 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 milieu in diabetic animals may be due to active suppression rather than to athrepsis.