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

✍ Scribed by Shivaprakash Gangappa; Shilpa P. Deshpande; Barry T. Rouse

• Publisher: John Wiley and Sons
• Year: 1999
• Tongue: English
• Weight: 188 KB
• Volume: 29
• Category: Article
• ISSN: 0014-2980
• DOI: 10.1002/(sici)1521-4141(199911)29:11<3674::aid-immu3674>3.0.co;2-7

✦ Synopsis

Herpetic stromal keratitis (HSK) is an immunopathological lesion involving herpes simplex virus (HSV) infection and CD4 + T cells of the Th1 phenotype, but the nature of the target antigens which drive HSK remains uncertain. In the present report we show that ovalbumin TCR-transgenic mice backcrossed to SCID mice unable to recognize HSV show clinical signs of HSK but die of viral encephalitis before the lesions become severe. However, passive transfer of anti-HSV serum at 24 h clears virus and affords protection from both HSK lesions and death. Adoptive transfer of CD8 + T cells at 72 h usually conferred protection but animals developed severe corneal pathology by 3 weeks post infection. At this time viral antigens were not demonstrable in 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 bystander activation of CD4 + T cells in a virus-induced inflammatory milieu. This mechanism of immunoinflammation may represent an important component of any lesion which involves CD4 + T cells.