Morrison W I, Murray M, Bovell D L
Lab Invest. 1981 Dec;45(6):547-57.
The response within the different cellular compartments of the spleen in mice infected with Trypanosoma congolense was evaluated using histologic and cytologic methods and immunofluorescence to detect intracellular and cell surface immunoglobulin. The isolate of T. congolense used produces a chronic infection in C3H/He mice leading to death 40 to 70 days after inoculation. Previous studies had shown that this infection resulted in a marked immunodepression as judged by a range of in vitro assays of splenic cellular responses. It was found that the splenic cellular changes occurred in two phases. First, coincident with and following the first peak of parasitemia, there was a marked proliferative phase characterized by widespread hyperplasia of the white pulp with the production of large numbers of plasma cells and an expansion of the erythropoietic component of the red pulp. During this period, there was a marked decrease in the intensity of staining for surface Ig on cells of the follicular regions of the white pulp. Following the initial proliferative changes, a more protracted phase ensued during which, although the proliferative activity continued, there was a gradual disorganization of the white pulp with eventual lymphoid depletion. This was accompanied by a progressive expansion of the red pulp due to increased numbers of erythropoietic cells and to a lesser extent granulopoietic cells and macrophages. At the same time, there was a gradual decrease in the number of plasma cells found in the red pulp, although many were still present in the periarteriolar regions. The end result of these changes was an approximately 17-fold increase in total splenic cellularity of which erythropoietic cells contributed more than 50 per cent, and lymphocytes were reduced in absolute numbers to below control levels. A striking feature during both phases of the infection was the lack of discrete germinal centers.
利用组织学、细胞学方法及免疫荧光技术检测细胞内和细胞表面免疫球蛋白,对感染刚果锥虫的小鼠脾脏不同细胞区室的反应进行了评估。所使用的刚果锥虫分离株在C3H/He小鼠中引起慢性感染,接种后40至70天导致死亡。先前的研究表明,通过一系列脾细胞反应的体外检测判断,这种感染导致明显的免疫抑制。发现脾脏细胞变化分为两个阶段。首先,与寄生虫血症的第一个峰值同时出现并在其之后,有一个明显的增殖阶段,其特征是白髓广泛增生,产生大量浆细胞,红髓的造血成分扩大。在此期间,白髓滤泡区细胞表面Ig的染色强度明显降低。在最初的增殖变化之后,接着是一个更持久的阶段,在此期间,虽然增殖活动持续存在,但白髓逐渐紊乱,最终淋巴细胞耗竭。这伴随着红髓因造血细胞数量增加以及在较小程度上因粒细胞生成细胞和巨噬细胞数量增加而逐渐扩大。与此同时,红髓中发现的浆细胞数量逐渐减少,尽管许多仍存在于动脉周围区域。这些变化的最终结果是脾脏细胞总数增加约17倍,其中造血细胞占比超过50%,淋巴细胞绝对数量减少至低于对照水平。感染的两个阶段中一个显著特征是缺乏离散的生发中心。