Solley G O, Gleich G J, Jordon R E, Schroeter A L
Monogr Allergy. 1977;12:179-88.
IgE antibodies can produce a late inflammatory response 6--12 h after allergen challenge which is characterized by diffuse edema, erythema, pruritus, tenderness and heat. That IgE is involved in inducing the late reaction was shown by the abolition of both immediate and late responses by passive transfer tests: (1) by heating atopic serum at 56 degrees C for 4 h; (2) by removing IgE from the atopic serum by a solid phase anti-IgE immunoabsorbent, and (3) by competitively inhibiting the binding of IgE antibodies to cells by an IgE myeloma protein. Also, both responses were induced by affinity chromatography-purified IgE antibody followed by antigenic challenge. Very similar lesions could be induced by intradermal injection of Compound 48/80. The late phase is characterized by edema and a mixed cellular infiltration, predominantly lymphocytic but also containing eosinophils, neutrophils and basophils. Direct immunofluorescent staining did not show deposition of immunoglobulins or complement components, except IgM in two of 15 and C3 in one of 15 patients, respectively.
IgE抗体可在变应原激发后6 - 12小时产生迟发性炎症反应,其特征为弥漫性水肿、红斑、瘙痒、压痛和发热。被动转移试验显示IgE参与迟发性反应的诱导:(1)将特应性血清在56℃加热4小时;(2)通过固相抗IgE免疫吸附剂从特应性血清中去除IgE;(3)用IgE骨髓瘤蛋白竞争性抑制IgE抗体与细胞的结合。此外,亲和层析纯化的IgE抗体继以抗原激发可诱导两种反应。皮内注射化合物48/80可诱发非常相似的损害。迟发期的特征为水肿和混合性细胞浸润,主要为淋巴细胞,但也含有嗜酸性粒细胞、中性粒细胞和嗜碱性粒细胞。直接免疫荧光染色未显示免疫球蛋白或补体成分的沉积,仅15例患者中的2例有IgM沉积,15例患者中的1例有C3沉积。