Scandinavian journal of rheumatology · 1976
Cell-mediated immune response to gonococcal antigen in uro-arthritis (Reiter's disease): (a) inhibition of migration of sensitised human lymphocytes, (b) lymphocyte transformation in vitro measured by 14C-thymidine uptake.
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.
Rosenthal L
Аннотация
Attempts have been made by in vitro methods to demonstrate the presence of a cell-mediated immune response to the gonococcus in human peripheral leukocytes. Leukocyte-migration tests in the presence of gonococcal antigen were performed in 34 patients with uro-arthritis (Reiter's disease), in 18 patients with newly developed gonorrhoea without joint manifestations, and in 34 controls (blood donors). In the patients with uncomplicated gonorrhoea the mean migration index (MI) was generally the same as in the healthy controls. A MI below 0.75 was noted in 21 of 34 cases of uro-arthritis. The number of cases with inhibited migration rose parallel with the duration of the disease and the presence of prostatis. Antigen-induced lymphocyte transformation was also studied by quantitation of the 14C-thymidine uptake in cell cultures. Studies were made in three groups of patients, one group with uroarthritis, one with gonococcal urethritis, and one with gonococcal septicaemia, and also in healthy controls. The lymphocyte stimulation induced by gonococcal antigen was significantly greater in uro-arthritis patients with known gonococcal infection (0.01less than p greater than 0.05) than in healthy controls. No difference in DNA synthesis was noted between patients with uncomplicated gonorrhoea and healthy controls, while the gonococcal septicaemia patients demonstrated a poor cellular immune response.