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-gamma production in Th1 responder strains such as C57BL/6 contributes to corneal perforation, while IL-18-driven IFN-gamma 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.