Varikuti Sanjay, Natarajan Gayathri, Oghumu Steve, Sperling Rachel H, Moretti Ellen, Stock James, Papenfuss Tracey L, Satoskar Abhay R
Department of Pathology, Wexner Medical Center, The Ohio State University, Columbus, OH, USA.
Department of Microbiology, The Ohio State University, Columbus, OH, USA.
Cell Immunol. 2016 Nov;309:61-68. doi: 10.1016/j.cellimm.2016.08.016. Epub 2016 Sep 6.
The outcome of visceral leishmaniasis, caused by parasite Leishmania donovani, depends on the recruitment of leishmanicidal Th1 cells. Chemokine receptor CXCR3, preferentially expressed by Th1 cells, is critical for migration of these T cells during infection. During chronic VL, there is a decrease in the presence of CXCR3-expressing CD4 T cells in the spleen, which is associated with high parasitic burden in this organ. We therefore examined whether T cell-specific expression of CXCR3 in mice (CXCR3) would promote resistance to VL. L. donovani infected CXCR3 mice showed increased accumulation of T cells in the spleens compared to WT littermates (CXCR3). However, CXCR3 T cells from CXCR3 mice showed low CD69 expression and these mice developed fewer granulomas. Additionally, both groups of mice showed similar cytokine profiles and parasitic burdens during the course of infection. In summary, although T cell-specific expression of CXCR3 promoted the accumulation of CXCR3-expressing T cells during L. donovani infection, this did not enhance resistance to VL.
由杜氏利什曼原虫寄生虫引起的内脏利什曼病的结果取决于杀利什曼原虫的Th1细胞的募集。趋化因子受体CXCR3优先由Th1细胞表达，对于这些T细胞在感染期间的迁移至关重要。在慢性内脏利什曼病期间，脾脏中表达CXCR3的CD4 T细胞数量减少，这与该器官中的高寄生虫负荷相关。因此，我们研究了小鼠中CXCR3的T细胞特异性表达（CXCR3）是否会促进对内脏利什曼病的抗性。与野生型同窝小鼠（CXCR3）相比，感染杜氏利什曼原虫的CXCR3小鼠脾脏中T细胞的积累增加。然而，来自CXCR3小鼠的CXCR3 T细胞显示出低CD69表达，并且这些小鼠形成的肉芽肿较少。此外，两组小鼠在感染过程中显示出相似的细胞因子谱和寄生虫负荷。总之，尽管CXCR3的T细胞特异性表达在杜氏利什曼原虫感染期间促进了表达CXCR3的T细胞的积累，但这并未增强对内脏利什曼病的抗性。
