Alleviation of IgE-mediated immune reactions in hypoinsulinaemic and hyperglycaemic mice.

Alloxan diabetic mice do not easily develop anaphylactic shock, and formation of IgE antibodies to sensitizing antigen almost ceases in these animals. Also, mice sensitized as normoglycaemic and then made diabetic are to a great degree protected from anaphylaxis, although they form minute but measureable amounts of IgE antibodies. Immune cells transferred into diabetic mice lose their ability to form IgE, while cells from immune diabetic mice, which in the hypoinsulinaemic milieu of donors do not synthesize appreciable amounts of IgE, regain this ability upon transfer into normal recipients. We conclude that the IgE response is very insulin-dependent and that insulin deficiency affects IgE-forming cells directly or indirectly via its influence on T helper cells. In the current study we also considered whether hyperglycaemia may influence the effector stage of anaphylactic reactions. To test this, massive doses of glucose were given to normoglycaemic mice, which increased their blood glucose level to that seen in diabetic mice and prevented local anaphylactic reactions when these mice were injected with monoclonal IgE antibody and challenged locally with antigen.