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Systemic Mycobacterium kansasii infection and regulation of the alloantigenic response.

机译:系统性堪萨斯分枝杆菌感染和同种抗原反应的调节。

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Specific-pathogen-free B6D2 F1 hybrid mice were infected intravenously with 10(7) to 10(8) viable Mycobacterium kansasii cells. The growth of the five test strains in vivo was correlated with the level of delayed hypersensitivity to a cytoplasmic protein antigen injected into the footpad. M. kansasii TMC no. 1201 and 1203 gave rise to persisting systemic infections with an early delayed hypersensitivity response (day 7) followed by a profound anergy to the cytoplasmic protein antigen injections. Strains 1204, 1214, and 1217 declined in viability relatively rapidly and failed to induce detectable levels of delayed hypersensitivity. Spleens harvested from mice infected 20 to 30 days earlier with 10(8) M. kansasii 1203 cells contained a T-cell subpopulation capable of suppressing mixed lymphocyte reactions between normal B6D2 and C3H(He) cells. On the other hand, splenic T-cells taken from M. kansasii 1214-infected mice enhanced, rather than suppressed, the indicator mixed lymphocyte reactions. The kinetics of stimulator-suppressor T-cell production within the spleens of the heavily infected mice differed as the two contrasting M. kansasii infections progressed. Such cellular interactions could well be responsible for the observed persistence of the systemic M. kansasii 1203 infection.
机译:无特异性病原体的B6D2 F1杂种小鼠经静脉内感染10(7)至10(8)个堪萨斯分枝杆菌活细胞。五个测试菌株在体内的生长与对注射到脚垫中的细胞质蛋白抗原的迟发型超敏反应水平相关。堪萨斯M. 1201和1203引起持续的全身感染,并有早期迟发的超敏反应(第7天),随后对细胞质蛋白抗原注射产生了严重的反应。菌株1204、1214和1217的存活力相对迅速地下降并且不能诱导可检测到的水平的迟发型超敏反应。从20到30天前感染10(8)堪萨斯分枝杆菌1203细胞的小鼠收获的脾脏包含能够抑制正常B6D2和C3H(He)细胞之间混合淋巴细胞反应的T细胞亚群。另一方面,取自堪萨斯州1214感染小鼠的脾脏T细胞增强而不是抑制了指标混合淋巴细胞反应。重度感染小鼠脾脏中刺激抑制性T细胞产生的动力学随着两种堪萨斯分枝杆菌感染的发展而有所不同。这种细胞相互作用很可能是观察到的全身性堪萨斯分枝杆菌1203感染的持续原因。

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