Bystander activation of CD4(+) T cells can represent an exclusive means ofimmunopathology in a virus infection

Herpetic stromal keratitis (HSK) is an immunopathological lesion involving herpes simplex virus (HSV) infection and CD4(+) T cells of the Th1 phenotyp e, but the nature of the target antigens which drive HSK remains uncertain. In the present report we show that ovalbumin TCR-transgenic mice backcross ed to SCID mice unable to recognize HSV show clinical signs of HSK but die of viral encephalitis before the lesions become severe. However, passive tr ansfer of anti-HSV serum at 24 h clears virus and affords protection from b oth HSK lesions and death. Adoptive transfer of CD8(+) T cells at 72 h usua lly conferred protection but animals developed severe corneal pathology by 3 weeks post infection. At this time viral antigens were not demonstrable i n the cornea and the T cells in the inflammatory lesions were CD4(+)KJ1-26. 1 idiotype positive, i.e. OVA peptide specific. These results indicate byst ander activation of CD4(+) T cells in a virus-induced inflammatory milieu. This mechanism of immunoinflammation may represent an important component o f any lesion which involves CD4(+) T cells.