Duffey L M, Albright J W, Albright J F
Exp Parasitol. 1985 Jun;59(3):375-89. doi: 10.1016/0014-4894(85)90093-1.
Cells of the hemocytic and lymphoreticular series located in the blood, bone marrow, spleen, and peritoneal space have been analyzed throughout the course of Trypanosoma musculi infections of intact and splenectomized C3H female mice. Following an early (within 2 days after trypanosome inoculation intraperitoneally) shift of leukocytes from the blood to the peritoneal space, there occurred a more gradual, prolonged infusion of leukocytes into the peritoneal space, the primary site of infection, that continued until the infection was terminated. There was intense cytogeneractive activity in the spleen that included erythrocytes, lymphocytes, myelocytes, and megakaryocytes. The marrow became primarily a site of monocytopoiesis and, to some extent, of lymphopoiesis. During the first 8 days (approximately) of infection, there was a decline in mature erythrocytes in the blood (the well-known anemia) and development of a profound thrombocytopenia. In splenectomized mice, the depletion of these elements continued unabated until the mice died; the marrow of infected, splenectomized mice failed to provide these elements, as was also the case in intact mice. In the peritoneal space, the intense battle between leukocytes and trypanosomes was reflected in a gradual, impressive rise in the number of dead and fatigued cells and, late in infection, in the development of ascites. Both of these abnormal conditions disappeared shortly after cure of the infection. We conclude that infections of mice with T. musculi result in dedication of the entire lymphoreticular system to the generation of cells that are exported to the peritoneal space to combat the major infection the occurs in that locale. This is consistent with the evidence that the belated immune elimination of T. musculi is a cell-mediated (probably antibody-dependent) process. The disruption of the normal histoarchitecture, the shift in the normal proportions of cells and in cells of different degrees of maturity, and probably, a block imposed on precursor cell maturation, account to a large extent for the well-known failure of immune responses commonly associated with trypanosome infections.
在完整的和脾切除的C3H雌性小鼠感染鼠锥虫的整个过程中，对位于血液、骨髓、脾脏和腹腔的血细胞和淋巴网状细胞系的细胞进行了分析。在早期（腹腔内接种锥虫后2天内）白细胞从血液转移至腹腔后，白细胞逐渐、持续地注入感染的主要部位腹腔，这一过程一直持续到感染结束。脾脏中有强烈的细胞生成活性，包括红细胞、淋巴细胞、髓细胞和巨核细胞。骨髓主要成为单核细胞生成的部位，在一定程度上也是淋巴细胞生成的部位。在感染的最初8天（约），血液中成熟红细胞数量下降（即众所周知的贫血），并出现严重的血小板减少。在脾切除的小鼠中，这些成分的消耗持续不减直至小鼠死亡；感染的脾切除小鼠的骨髓无法提供这些成分，完整小鼠的情况也是如此。在腹腔中，白细胞与锥虫之间的激烈战斗表现为死亡和疲惫细胞数量逐渐显著增加，在感染后期则表现为腹水的形成。感染治愈后不久，这两种异常情况均消失。我们得出结论，小鼠感染鼠锥虫会导致整个淋巴网状系统致力于生成输出至腹腔的细胞，以对抗该部位发生的主要感染。这与鼠锥虫延迟的免疫清除是细胞介导（可能是抗体依赖）过程的证据一致。正常组织结构的破坏、细胞正常比例和不同成熟度细胞的变化，以及可能对前体细胞成熟的阻滞，在很大程度上解释了与锥虫感染相关的免疫反应常见的众所周知的失败。
