Mycobacterium marinum strains 1218 and 1219 were inoculated into the hind footpads of T-cell-depleted specific pathogen-free C57B1/6 mice, and the growth and survival of the organisms at the site of injection, the draining popliteal lymph node, and the spleen and lung were quantitated for up to 70 days. T-cell depletion largely ablated the normal cell-mediated antituberculous response to the M. marinum population. The mice were able to control the further growth of the inoculum within the footpad only after it had reached 5 to 10 times that present in the normal controls. The high temperature-adapted strain (37 C; strain no. 1218) induced an increasing infection in the liver, spleen, and lungs of the THXB mice, and the infection eventually spread to the opposite footpad and to the tail skin. Strain 1219 gave rise to considerable systemic involvement in the THXB host despite its inability to survive at 37 C, but the size of the splenic and lung populations was considerably lower than in the 1218-infected animals. Both M. marinum infections persisted in the tissues of the T-cell-depleted mice with no indication of a cell-mediated immune response. Footpad swelling in the M. marinum-infected mice was not greatly reduced by T-cell depletion, and, if anything, tended to persist at high levels long after the swelling of the control feet had gone into a decline. On the other hand, incorporation of tritiated thymidine by cells within the infected footpads, the draining lymph node, and the spleen was considerably reduced in the T-cell-depleted host compared with control values. Late in the infection, there was a significant increase in the amount of label taken up by the cells in the footpads of the T-cell-depleted host.
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机译：将马内杆菌菌株1218和1219接种到T细胞耗尽的特异性病原体C57B1 / 6小鼠的后脚垫中，以及在注射液部位，排出的popliteal淋巴结和脾脏生物的生长和存活和肺量定量长达70天。 T细胞耗竭大部分烧蚀于对M. Marinum群体的正常细胞介导的抗胆囊反应。在正常对照中达到5至10倍后，小鼠能够控制脚板内接种物的进一步生长。高温适应菌株（37℃;菌株NO.1218）诱导THXB小鼠的肝脏，脾脏和肺部的增加感染，并且感染最终蔓延到相对的脚板和尾部皮肤。尽管它无法在37℃下存活，但菌株1219在THXB宿主中产生了相当大的全身培养，但是脾和肺种群的大小比1218感染动物的大小相当低。 M. M.Marinum感染仍然存在于T细胞耗尽小鼠的组织中，没有指示细胞介导的免疫应答。在M. marinum-cerved小鼠中肿胀的脚板膨胀并没有大大减少T细胞枯萎病，如果有任何东西，在对照脚肿胀后持续的高水平趋于延长，往往持续下降。另一方面，与对照值相比，T细胞耗尽的宿主中，通过感染的潮脚板，排水淋巴结和脾脏中的细胞掺入氚化的胸苷。在感染后期，细胞在T细胞耗尽宿主的脚间中占据的标签量显着增加。
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