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

Abstract 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)-d...

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Bibliographic Details
Published in:Journal of neuroimmunology 2011-05, Vol.234 (1), p.103-108
Main Authors: Wuest, Todd R, Thapa, Manoj, Zheng, Min, Carr, Daniel J.J
Format: Article
Language:English
Subjects:
Allergy and Immunology
Animals
Brain Stem - metabolism
Brain Stem - pathology
Brain Stem - virology
CD4-Positive T-Lymphocytes - metabolism
Chemokine CXCL10 - deficiency
Chemokine production
Chemokines - metabolism
CXCL10
Disease Models, Animal
Flow Cytometry - methods
Hematopoietic Stem Cell Transplantation - methods
Hematopoietic Stem Cells - physiology
Herpes Simplex - pathology
Herpes Simplex - surgery
Herpes simplex virus 1
Herpesvirus 1, Human
HSV-1
Killer Cells, Natural - metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
Mouse chimera
Neurology
T cell chemotaxis
Trigeminal Ganglion - metabolism
Trigeminal Ganglion - pathology
Trigeminal Ganglion - virology
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Summary:Abstract 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.
ISSN:0165-5728
1872-8421
DOI:10.1016/j.jneuroim.2011.03.006