Control of viral immunoinflammatory lesions by manipulating CD200:CD200 receptor interaction

Previous investigators have demonstrated that the CD200:Fc that engages CD200 receptors (CD200R) shows promise as an immunosuppressive and anti-inflammatory reagent. In this report, we evaluate the use of CD200:Fc to control a viral induced immunoinflammatory reactions caused by ocular infection with herpes simplex virus (HSV). Our results show that HSV infection causes invasion of the cornea by CD200R(+) cells most of which were CD11b(+) cells. Systemic administration of CD200:Fc, starting at 5 days post infection (p.i.), resulted in diminished incidence and severity of lesions compared to controls. Splenocytes isolated from treated animals showed reduced IL-12 and IFN-gamma responses when stimulated in vitro and ex vivo. Treated animals also had increased frequencies of Foxp3(+) regulatory T cells in both the cornea and draining lymph nodes perhaps contributing also to the control of the corneal immunopathology. Treatment of animals in the chronic phase was minimally effective. Our data are the first to demonstrate the use of CD200R stimulation to control lesion severity in a viral induced inflammatory disease.