共 33 条
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.
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页码:103 / 108
页数:6
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