Pathogenesis of herpes simplex virus-induced ocular immunoinflammatory lesions in B-cell-deficient mice.
The role of B cells and humoral immunity in herpes simplex virus (HSV) ocular infections was studied in immunoglobulin mu chain gene-targeted B-cell-deficient mice (muK/O). At doses of virus well tolerated by immunocompetent mice, heightened susceptibility of muK/O mice to herpetic encephalitis as well as to herpetic stromal keratitis (HSK) was observed. An explanation was sought for the increased severity of HSK in the muK/O mice. First, the lack of antibody responses in muK/O mice resulted in longer viral persistence and dissemination to the corneal stroma, the site of inflammation. Prolonged virus expression in the corneal stroma was suggested to cause bystander activation of Th1-type CD4(+) T cells, further contributing to the severity of HSK lesion expression in muK/O mice. Second, muK/O mice generated minimal Th2 cytokine responses compared to wild-type mice. Such responses might serve to downregulate the severity of Th1-mediated HSK lesions.[1]References
- Pathogenesis of herpes simplex virus-induced ocular immunoinflammatory lesions in B-cell-deficient mice. Deshpande, S.P., Zheng, M., Daheshia, M., Rouse, B.T. J. Virol. (2000) [Pubmed]
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