Howdle P D, Blair Zajdel M E, Smart C J, Trejdosiewicz L K, Blair G E, Losowky M S
Dept. of Medicine, St. James's University Hospital, Leeds, U.K.
Scand J Gastroenterol. 1989 Apr;24(3):282-6. doi: 10.3109/00365528909093047.
The description of an amino acid sequence homology between the E1B-58-kDa protein of adenovirus 12 and gliadin has led to the suggestion that previous infection by this virus and subsequent exposure to gliadin could trigger the development of coeliac disease in susceptible individuals as a result of immunologic cross-reactivity. We have sought to measure specific antibodies to the E1B-58-kDa protein in 23 coeliac patients and 10 normal subjects. The sera were analysed by radioimmunoprecipitation with metabolically labelled adenovirus-12-transformed rat cells (which express the E1B-58-kDa protein), followed by separation on polyacrylamide gels. None of the coeliac sera had evidence of antibodies to the E1B-58-kDa protein. These data suggest that coeliac patients show little evidence of humoral immunity to the specific adenovirus 12 E1B-58-kDa protein implicated in the aetiology of coeliac disease.
腺病毒12的E1B-58-kDa蛋白与麦醇溶蛋白之间氨基酸序列同源性的描述,提示先前感染该病毒以及随后接触麦醇溶蛋白,可能会因免疫交叉反应,在易感个体中引发乳糜泻。我们试图检测23例乳糜泻患者和10名正常受试者体内针对E1B-58-kDa蛋白的特异性抗体。通过用代谢标记的腺病毒12转化大鼠细胞(表达E1B-58-kDa蛋白)进行放射免疫沉淀分析血清,随后在聚丙烯酰胺凝胶上进行分离。没有一份乳糜泻患者的血清有针对E1B-58-kDa蛋白的抗体证据。这些数据表明,乳糜泻患者几乎没有针对与乳糜泻病因相关的特异性腺病毒12 E1B-58-kDa蛋白的体液免疫证据。