Abstract
CXCL10 and blood-brain barrier modulation in rabies virus infection.
Highlights
Rabies is a lethal neurological disease caused by the neurotropic rabies virus (RABV)
2) CXCL10 mediates the recruitment of CD4+ T-cells into the central nervous system (CNS). 3) CXCL10 mediates the differentiation of CD4+ T cells into 4a) IFN-γ secreting Th1 cells, which could further boost the induction of CXCL10 through positive feedback, and 4b) IL17 secreting Th17 cells, alters the tight junction (TJ) proteins resulting in blood-brain barrier (BBB) breakdown
In addition to IL-17, the BBB permeability enhancement is reinforced by amplification of CXCL10 production by IFN-γ secreted by Th1 cells through positive feedback
Summary
Rabies is a lethal neurological disease caused by the neurotropic rabies virus (RABV). In these issues of the Journal of virology, Chai et al, investigated the mechanism by which attenuated RABV infection initiates BBB permeability enhancement in mice [4, 5]. It was observed that the attenuated RABV infection in mice enhances BBB permeability by reducing the TJ proteins and inducing infiltration of inflammatory cells into the CNS.
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