Sera of 50% of persons extremely sensitive and of 30% of persons moderately sensitive to milk had heat-labile reaginic antibodies conferring passive cutaneous anaphylactic sensitivity on monkeys for 24 hr. More persons in each group had IgE antibodies that bound radio-isotope labelled β-lactoglobulin and passively sensitized monkey basophils for anaphylactic degranulation.
These tests, however, are not certain evidence of clinical allergy, because of the sera of nineteen topic children, three mediated monkey PCA tests and five had γE anti-$bt-lactoglobulin antibodies detected by antigen binding or basophil degranulation, though the serum donors were not clinically allergic to milk. Similarly few normal, milk-tolerant adults also had γE anti-β-lactoglobulin antibodies.
Sera of nine children with milk-induced gastroenteritis occurring 12–36 hr after exposure had no anti-milk reagins, and only one had γE binding β-lactoglobulin. This allergy may be mediated by heat-stable IgG antibodies, because three sera conferred milk sensitivity on monkey skin for 4 hr and two others for 2 hr. The three sera had high titres of IgG agglutinins, one to β-lactoglobulin, one to α-lactalbumin and one to casein. All three fixed complement in the presence of milk, and one had precipitins. They did not passively sensitize human mast cells or monkey basophils for anaphylactic degranulation, but they prepared human lung for anaphylactic release of hist-amine, though in small amounts compared to that released from lung prepared with reagins.
The sera of two of three cases of cot death had IgG antibodies with similar properties.