Allergic sensitisation of human lung fragments prevented by saturation of IgE binding sites

Abstract

PASSIVELY sensitised chopped human lung fragments release mediators of immediate hypersensitivity when challenged with appropriate antigens¹. Antigen triggers the release of mediators from mast cells or basophils by coupling of neighbouring surface IgE antibody molecules sharing the same antigen specificity². Release of mediators should therefore be unlikely if specific IgE molecules are sparsely distributed on cell surfaces, as in normal non-allergic people, or if surface receptors are densely occupied by IgE molecules with other specificities. Humans harbouring certain parasites develop high IgE levels³, and epidemiological evidence suggests that allergic disorders such as hayfever or pollen asthma are rare in heavily parasitised populations^4,5. It is not known whether IgE induced in man by parasite infestation is directed specifically against parasite antigens, or whether it represents nonspecific potentiation of IgE production against many different antigens, as demonstrated in the rat Nippostrongylus model⁶. Here we show that human lung fragments first exposed to IgE-rich serum from West African residents become resistant to further passive sensitisation with serum containing grass pollen-specific IgE.