A novel early-type hypersensitivity (ETH) reaction, manifested as capillary congestion, increase of vasopermeability, and plasma protein leakage, can be induced within 1 h after challenge of antigen-sensitized mice. The mediators involved in ETH varied among different strains of mice. The poly(Glu60Ala30Tyr10) (GAT)-induced ETH in BALB/c mice was blocked by diphenhydramine (histamine H1 antagonist) and ketanserine (serotonin antagonist), but not by cimetidine (histamine H2 antagonist). These results indicate that both histamine and serotonin are involved, and that the histamine effect is mediated through a H1 receptor. Meanwhile, GAT-induced ETH in B6 mice was inhibited by anti-TNFα antibody suggesting that TNFα is involved. The mice can be classified into either histamine or TNFα type based on the pattern of mediator involved in ETH. A/J and CBA strains as well as BALB/c mice were classified as histamine type while A.TL, B10.BR, and C3H/He in addition to B6 mice were TNFα type. The observation that GAT-induced ETH in (BALB/ c × B6)F1 mice was inhibited by both diphenhydramine and anti-TNFα suggests that the mediation of the actions of histamine or TNFα by GAT was genetically controlled and inherited as the dominant trait in (BALB/c × B6)F1 mice. ETH could be passively transferred by heat (56 °C, 4 h)-treated anti-GAT sera. Sera derived from the histamine type transferred ETH across the type barrier and histamine was the mediator, irrespective of the type of the recipient. However, sera derived from TNFα type only transferred ETH to the mice of the same TNFα type and TNFα was the mediator.
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