Das G, Vohra H, Rao K, Saha B, Mishra G C
National Center for Cell Sciences, Ganeshkhind, Pune, India.
Scand J Immunol. 1999 Mar;49(3):307-10. doi: 10.1046/j.1365-3083.1999.00486.x.
The disease visceral leishmaniasis is caused by a protozoan parasite, Leishmania donovani and is characterized by depressed cell-mediated immunity (CMI) and unhindered parasite growth in a susceptible host. The opposite trend is observed in a resistant host. However, the mechanism of this loss of CMI during the progressive disease is unknown as yet. In this report, we demonstrate that more than 40% of CD4+ T cells from a susceptible host undergo apoptosis resulting in a significant decrease in interleukin (IL)-2 and interferon (IFN)-gamma secretion, leaving IL-4 secretion unaffected. These changes are not apparent in the case of CD4+ T cells derived from a resistant host. The data reported here suggest that experimental Leishmania donovani infection leads to selective deletion of the IL-2 and IFN-gamma-secreting cells but not Th2-like cells in a susceptible but not a resistant host.
内脏利什曼病由原生动物寄生虫杜氏利什曼原虫引起，其特征是细胞介导免疫（CMI）受到抑制，且在易感宿主中寄生虫不受阻碍地生长。在抗性宿主中观察到相反的趋势。然而，在疾病进展过程中这种CMI丧失的机制尚不清楚。在本报告中，我们证明来自易感宿主的超过40%的CD4 + T细胞发生凋亡，导致白细胞介素（IL）-2和干扰素（IFN）-γ分泌显著减少，而IL-4分泌不受影响。对于来自抗性宿主的CD4 + T细胞，这些变化并不明显。此处报告的数据表明，实验性杜氏利什曼原虫感染导致易感但非抗性宿主中分泌IL-2和IFN-γ的细胞被选择性清除，但不影响Th2样细胞。
