Mouse splenic CD4+ and CD8+ T cells undergo extensive apoptosis during a Plasmodium chabaudi chabaudi AS infection

Mouse splenic CD4+ and CD8+ T cells undergo extensive apoptosis during a Plasmodium chabaudi chabaudi AS infection
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DOI:
10.1046/j.1365-3024.2001.00422.x
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发表时间:
2001-12-01
影响因子:
2.2
通讯作者:
Favila-Castillo, L
Favila-Castillo, L
中科院分区:
医学4区
文献类型:
--
作者:
Sanchez-Torres, L;Rodriguez-Ropon, A;Favila-Castillo, L

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研究了感染夏氏疟原虫(Plasmodiumchabaudi-chabaudiAS)的CB 6 F1小鼠脾细胞悬液中凋亡淋巴细胞的存在和表型。发现高水平的凋亡细胞,与高寄生虫血症和脾肿大相关。同时伴有脾白色髓扩张、排列紊乱。寄生虫血症清除后,细胞凋亡水平降低,但仍高于正常小鼠。此时,脾脏体积缩小,白色髓收缩并重新排列。寄生虫血症时,受凋亡影响最大的细胞是CD 4(+)T细胞,其次是CD 8(+)T细胞,B220(+)B细胞的影响较小。当寄生虫血症清除后,CD 8(+)T细胞和B220(+)B细胞恢复到凋亡的基础水平,而CD 4(+)T细胞的凋亡水平仍高于正常小鼠。在感染的BALB/c小鼠中发现了类似的淋巴细胞亚群凋亡模式,尽管事实上,对于该小鼠模型,已报道B细胞是最受凋亡影响的细胞。我们认为,当寄生虫血症仍然很高时,CD 4(+)T细胞的高水平凋亡并不容易用免疫应答下调的正常机制来解释。
The presence and phenotype of apoptotic lymphocytes was studied in spleen cell suspensions taken from CB6F1 mice infected with Plasmodium chabaudi chabaudi AS. High levels of apoptotic cells were found, associated with high parasitaemias and splenomegaly. This was also accompanied by expansion and disarray of spleen white pulp. Apoptosis levels lowered when parasitaemia was cleared, but were still higher than in normal mice. At this time, the spleen was diminishing in size and the white pulp was contracting and rearranging, When parasitaemia was patent, the cells most affected by apoptosis were CD4(+) T cells followed by CD8(+) T cells, and to a lesser extent B220(+) B cells. When parasitaemia was cleared, CD8(+) T cells and B220(+) B cells returned to basal levels of apoptosis, while CD4(+) T cells still had higher apoptosis levels than normal mice. A similar pattern of lymphocyte subpopulation apoptosis was found in infected BALB/c mice, despite the fact that, for this mouse model, it has been reported that B cells are the cells that are most affected by apoptosis. We consider that the high levels of apoptosis in CD4(+) T cells when parasitaemias are still high are not easily explained by a normal mechanism of down regulation of the immune response.