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http://purl.uniprot.org/citations/17724202http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17724202http://www.w3.org/2000/01/rdf-schema#comment"

Purpose

The host inflammatory response to ocular infection with herpes simplex virus (HSV) can be either protective, with disease-free survival, or it can promote diseases such as HSV corneal disease (or herpes stromal keratitis [HSK] in humans) and encephalitis (HSE), depending on mouse strain. The role of CXCR3 chemokine signaling in HSV-induced central nervous system (CNS) inflammation and corneal disease was evaluated, and responses in genetically susceptible and resistant strains of mice were contrasted.

Methods

Resistant C57BL/6J (B6) and susceptible 129S6 (129) mice were given monoclonal antibodies (mAbs) to neutralize the CXCR3 ligands monokine induced by interferon-gamma (MIG, CXCL9) and interferon inducible protein-10 (IP-10, CXCL10) during HSV infection. In addition, the development of HSV disease was monitored in CXCR3-null mutant mice derived from resistant (B6) and susceptible (BALB/c) strains. Inflammatory cells infiltrating the cornea and brain stem were isolated and stained for flow cytometric analysis.

Results

MIG and IP-10 were induced in nervous system tissue after HSV inoculation by the corneal route. HSV-infected 129 mice treated with MIG- or IP-10-neutralizing mAbs showed significantly enhanced survival compared with mice treated with control isotype antibody, whereas survival of the B6 mice was unaltered. Similarly, greater survival was observed for BALB.CXCR3(-/-) mice compared with control BALB/c mice. Reduced CNS inflammation was documented that extended to the cornea, such that HSV corneal disease severity was reduced in susceptible BALB.CXCR3(-/-). In contrast, although survival of B6 and B6.CXCR3(-/-) mice was indistinguishable, B6.CXCR3(-/-) mice developed more severe corneal and periocular skin disease.

Conclusions

The effects of CXCR3 signaling in HSV infection are strongly dependent on mouse strain."xsd:string
http://purl.uniprot.org/citations/17724202http://purl.org/dc/terms/identifier"doi:10.1167/iovs.07-0261"xsd:string
http://purl.uniprot.org/citations/17724202http://purl.uniprot.org/core/author"Wang M."xsd:string
http://purl.uniprot.org/citations/17724202http://purl.uniprot.org/core/author"Yang H.J."xsd:string
http://purl.uniprot.org/citations/17724202http://purl.uniprot.org/core/author"Lundberg P."xsd:string
http://purl.uniprot.org/citations/17724202http://purl.uniprot.org/core/author"Cantin E."xsd:string
http://purl.uniprot.org/citations/17724202http://purl.uniprot.org/core/author"Openshaw H."xsd:string
http://purl.uniprot.org/citations/17724202http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17724202http://purl.uniprot.org/core/name"Invest Ophthalmol Vis Sci"xsd:string
http://purl.uniprot.org/citations/17724202http://purl.uniprot.org/core/pages"4162-4170"xsd:string
http://purl.uniprot.org/citations/17724202http://purl.uniprot.org/core/title"Effects of CXCR3 signaling on development of fatal encephalitis and corneal and periocular skin disease in HSV-infected mice are mouse-strain dependent."xsd:string
http://purl.uniprot.org/citations/17724202http://purl.uniprot.org/core/volume"48"xsd:string
http://purl.uniprot.org/citations/17724202http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/17724202
http://purl.uniprot.org/citations/17724202http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/17724202
http://purl.uniprot.org/uniprot/#_O88410-mappedCitation-17724202http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17724202
http://purl.uniprot.org/uniprot/O88410http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/17724202