CXCL10 expressing hematopoietic-derived cells are requisite in defense against HSV-1 infection in the nervous system of CXCL10 deficient mice

被引:10
作者
Wuest, Todd R. [2 ]
Thapa, Manoj [2 ]
Zheng, Min
Carr, Daniel J. J. [1 ,2 ]
机构
[1] Univ Oklahoma, Hlth Sci Ctr, Dept Ophthalmol, Oklahoma City, OK 73104 USA
[2] Univ Oklahoma, Hlth Sci Ctr, Dept Microbiol & Immunol, Oklahoma City, OK 73104 USA
关键词
HSV-1; CXCL10; Chemokine production; Mouse chimera; T cell chemotaxis; HERPES-SIMPLEX-VIRUS; IMMUNE-RESPONSE; T-LYMPHOCYTES; BONE-MARROW; IFN-GAMMA; CHEMOKINES; RECRUITMENT; RECEPTOR; MICROGLIA; MIGRATION;
D O I
10.1016/j.jneuroim.2011.03.006
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The chemokine CXCL10 is crucial for the control of viral replication through the regulation of mobilization of antigen-specific T cells to sites of infection. CXCL10 is highly expressed both at sites of inflammation as well as constitutively within lymphoid organs by both bone marrow (BM)-derived and non-BM-derived cells. However, the relative immunologic importance of CXCL10 expressed by these divergent sources relative to HSV-1 infection is unknown. Using mouse chimeras reconstituted with either wild type or CXCL10 deficient mouse BM, we show BM-derived, radiation-sensitive cells from wild type mice were solely responsible for resistance to HSV-1 in the trigeminal ganglia and brain stem. The resistance was not reflected by a deficiency in the recruitment of effector cells to sites of inflammation or expression of chemokines or IFN-gamma and likely results from additional, yet-to-be-determined factors emanating from wild type. BM-derived cells. (C) 2011 Elsevier B.V. All rights reserved.
引用
收藏
页码:103 / 108
页数:6
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