Clinical and experimental immunology · 1969
The relative antigen-neutralizing capacity (avidity) of thyroglobulin antibodies in various thyroid diseases as measured by haemagglutination-inhibition with antibody-coated cells.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Hjort T
Аннотация
Human sera which in a haemagglutination test with thyroglobulin-coated cells revealed thyroglobulin-antibody titres of 55 or more were tested by a haemagglutination-inhibition technique with cells coated with highly purified rabbit antibody to human thyroglobulin. Theoretical considerations indicated that the titres obtained in this inhibition system would be influenced not only by the concentration of thyroglobulin-antibody, but also by the avidity of the antibody. Therefore, it should be possible to disclose differences in antibody avidity by comparing the inhibiting and agglutinating activity of the sera. Based on these assumptions, sera from twenty-four patients with lymphadenoid goitre were found generally to contain highly avid thyroglobulin antibodies, although a decrease in avidity could apparently occur during the disease. Similar findings were made with sera from twenty-three patients with primary myxoedema, whereas sera from twelve thyrotoxic patients yielded relatively weaker inhibition reactions and were of a significantly lower avidity. Antibodies of very low avidity were found in five of seven cases with a clinical diagnosis of non-toxic goitre (or in all five cases of histologically verified non-toxic goitre), in two of three patients with cancer of the thyroid, and in two patients with subacute thyroiditis. These differences in reactivity of the thyroglobulin-antibodies may refer to different pathogenic mechanisms eliciting the autosensitization.