1973 Volume 19 Issue 3Supplement2 Pages 451-457
It has been revealed by Ishizaka, et al. that IgE is a carrier of human reaginic antibodies, and anti-sera specific for human IgE induces erythema-wheal reaction in normal individuals when small amounts of anti-IgE are injected. The skin reaction is considered to be mediated by anti-sera combining with IgE on skin cells.
Injections with anti-IgE also produced reactions simi lar to atopic allergy in the normal skin, the mucous membrane of the oral cavity, trachea and conjunctiva in the present study. The tissues injected were removed and examined by light and electron microscope. The histological changes were characteristic in degranulation of the mast cell, local circulatory disturbance, edema, hypersecretion and eosinophilia. The ultrastructural examination revealed the endothelial vesiculation, dilatation of the interendothelial clefts, diapedesis of the plasma in the venules, and contraction of the arterioles. Furthermore, the specific granule of the eosinophil were changed markedly.
Animal model of atopic allergy was made in rats by sensitization with dinitrophenylated ascaris extracts. When anti-rat IgE serum was given, the peritoneal mast cells showed degranulations, and the microcirculation of the mesenterium was changed in the following chronological processes: 1 slowing down or stasis of the blood flow and aggulutination of the red cells: 2 plasma skimming and contraction of the arterioles: 3 recovery of the blood flow.
By injection with anti-IgE into varing tissues of human and rats, local atopic allergy were experimentally produced.
