Reviews for Immune Privilege in the Year 2010: Immune Privilege and Infection

Abstract

Advances in understanding host innate/adaptive immunity and abrogation of immune privilege in ocular viral and bacterial infections have been accomplished using animal models. In Pseudomonas aeruginosa keratitis, mouse models have shown that IL-12-driven IFN-γ production in Th1 responder strains such as C57BL/6 contributes to corneal perforation, while IL-18-driven IFN-γ production is associated with bacterial killing and less disease in Th2 responders (BALB/c). The role of neuropeptides, macrophages, and regulation of neutrophil apoptosis is discussed. The potentially blinding Th1 CD4 T-cell-mediated immunopathology referred to as herpes stromal keratitis (HSK) is characterized by breakdown of the normal barrier to blood and lymph angiogenesis in the cornea, a dramatic increase in mature professional antigen-presenting cells, and a heavy leukocytic infiltrate composed primarily of neutrophils. HSK is more frequent and severe in BALB/c than C57BL/6 mice, and varies in severity with the strain and dose of HSV-1 used to infect the cornea.

KEYWORDS::

• herpes simplex virus type 1 (HSV-1)
• lymph and blood angiogenesis
• neuropeptides
• neutrophils
• Pseudomonas aeruginosa
• Toll-like receptors

ACKNOWLEDGEMENTS

Support for this work was provided by NIH grants R01EY002986, R01EY16058, P30EY004068, and CIBA Vision (all to LDH) and R01EY05945, R01EY01035, P30EY08098, and an unrestricted grant from Research to Prevent Blindness (New York, NY) and the Eye and Ear Foundation of Pittsbutgh (all to RLH).

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.