Patrick M. Stuart

FasL, leukocytes and vascular modeling.

Therapeutic immunization with a virion host shutoff-defective, replication-incompetent herpes simplex virus type 1 strain limits recurrent herpetic ocular infection.

Therapeutic vaccination with vhs(-) herpes simplex virus reduces the severity of recurrent herpetic stromal keratitis in mice.

FasL-Fas interactions regulate neovascularization in the cornea.

Apoptosis, tolerance, and regulatory T cells--old wine, new wineskins.

Effect of metalloprotease inhibitors on corneal allograft survival.

CD8(+) T cells control corneal disease following ocular infection with herpes simplex virus type 1.

Interleukin-10 (IL-10) ameliorates corneal disease in a mouse model of recurrent herpetic keratitis.

Peripheral deletion of antigen-specific T cells leads to long-term tolerance mediated by CD8+ cytotoxic cells.

The role of Fas ligand as an effector molecule in corneal graft rejection.

The effects of aminoguanidine on primary and recurrent ocular herpes simplex virus infection.

CD8 T cells mediate transient herpes stromal keratitis in CD4-deficient mice.

CCL3 protects mice from corneal pathology during recurrent HSV-1 infection.

Interferon gamma is not required for recurrent herpetic stromal keratitis.

Delivery of Interferon-gamma by an adenovirus vector blocks herpes simplex virus Type 1 reactivation in vitro and in vivo independent of RNase L and double-stranded RNA-dependent protein kinase pathways.

Mice with mutations in Fas and Fas ligand demonstrate increased herpetic stromal keratitis following corneal infection with HSV-1.

Recurrent herpetic stromal keratitis in mice: a model for studying human HSK.