Lack of CXCR3 delays the development of hepatic inflammation but does not impair resistance to Leishmania donovani
Lack of CXCR3 delays the development of hepatic inflammation but does not impair resistance to Leishmania donovani
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DOI：
10.1086/516787
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发表时间：
2007-06-01
影响因子：
6.4
通讯作者：
Satoskar, Abhay R.
中科院分区：
文献类型：
--
作者：
Barbi, Joseph;Oghumu, Steve;Satoskar, Abhay R.
CXC趋化因子受体3（CXCR 3）配体CXCL 9和CXCL 10在感染杜氏利什曼原虫的小鼠和人类中以高水平产生，但它们对宿主抵抗杜氏利什曼原虫的贡献。多诺万尼不清楚。在这里，我们使用CXCR 3（-/-）小鼠，我们证明，虽然CXCR 3调节早期免疫细胞运输和肝脏炎症在L。donovani感染时，对L. donovani，不像L.少校CXCR 3（-/-）C57 BL/6小鼠在接种L. Donovani感染然而，它们能够产生有效的1型T辅助细胞反应，将T细胞募集到肝脏，并与CXCR 3（+/+）C57 BL/6小鼠一样有效地控制寄生虫生长。
CXC chemokine receptor 3 (CXCR3) ligands CXCL9 and CXCL10 are produced at high levels in mice and humans infected with Leishmania donovani, but their contribution to host resistance against L. donovani is not clear. Here, using CXCR3(-/-) mice, we demonstrate that, although CXCR3 regulates early immune cell trafficking and hepatic inflammation during L. donovani infection, it is not essential for immunity against L. donovani, unlike L. major. CXCR3 (-/-) C57BL/6 mice show a delayed onset of hepatic inflammation and granuloma formation after L. donovani infection. However, they mount an efficient T helper cell type 1 response, recruit T cells to the liver, and control parasite growth as efficiently as do CXCR3(+/+) C57BL/6 mice.