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Studies on the immunological disturbance in murine schistosomiasis japonica from the viewpoint of the interleukin cascade reaction.

机译:从白细胞介素级联反应的角度研究日本血吸虫病的免疫学障碍。

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摘要

We examined the mechanisms of disturbed T-lymphocyte function that occurred during Schistosoma japonicum infection of BALB/c mice from the viewpoint of the interleukin cascade reaction. Each point of the interleukin cascade reaction was examined. First, IL-1 production by adherent peritoneal or spleen cells, as a source of macrophages, was normal or rather enhanced during the infection, the values being 100-180% of the control. Secondly, proliferative response to exogenous IL-1 of thymocytes from S. japonicum-infected mice progressively decreased during 3-7 weeks of infection. Thirdly, IL-2 production of S. japonicum-infected mice was significantly inhibited, even at 2 weeks of infection, and the activity was 10-20% of the control at 5-8 weeks of infection. Diminished IL-2 production was not caused by suppressive factors, such as PGE2 or suppressor macrophages, or a decrease in the number of IL-2 producing T cells. Finally, the response to exogenous IL-2 in S. japonicum-infected mice was suppressed markedly by 4 weeks of infection, and the responsiveness was reduced to 20% of the control at 8 weeks of infection. The mechanisms of disturbances in T-cell functions in S. japonicum-infected mice are discussed.
机译:我们从白介素级联反应的角度检查了日本血吸虫感染BALB / c小鼠过程中发生的T淋巴细胞功能紊乱的机制。检查白介素级联反应的每个点。首先,在感染期间由粘附的腹膜或脾细胞作为巨噬细胞的来源产生的IL-1是正常的,或者甚至在感染过程中有所增强,其值为对照的100-180%。其次,在感染的3-7周内,日本血吸虫感染的小鼠对胸腺细胞外源IL-1的增殖反应逐渐降低。第三,即使在感染2周后,日本链球菌感染小鼠的IL-2产生也被显着抑制,并且在感染5-8周时其活性是对照的10-20%。 IL-2产生减少不是由抑制因素引起的,例如PGE2或抑制性巨噬细胞,或产生IL-2的T细胞数量减少。最后,感染日本血吸虫后4周,小鼠对外源IL-2的反应被显着抑制,感染8周时,其反应率降至对照组的20%。讨论了日本血吸虫感染小鼠的T细胞功能紊乱的机制。

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