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Shivaprakash Gangappa, Shilpa P. Deshpande, Barry T. Rouse; Bystander Activation of CD4+ T Cells Accounts for Herpetic Ocular Lesions. Invest. Ophthalmol. Vis. Sci. 2000;41(2):453-459.
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purpose. Stromal keratitis is an immunopathologic consequence of herpes simplex
virus (HSV) infection of the cornea. The lesion is immunopathologic,
but the identities of molecules that drive the reaction remain
unresolved. To exclude viral antigen recognition as a necessary step in
the disease process, ocular HSV infection was followed in Tg-RAG mice
(OVA-TCR transgenic mice crossed to RAG2-deficient mice) whose limited
T-cell repertoire did not include immune responsiveness to HSV.
methods. Mice with T-cell specificity to OVA peptide (Tg-RAG mice) as well
as control DO11.10 and BALB/c mice were infected with HSV on the
scarified cornea and subjected to clinical, histologic, and immunologic
analysis. To evaluate involvement of OVA-specific CD4+ T
cells in lesion development in Tg-RAG mice, monoclonal antibody to
CD4+ T cells was used for in vivo CD4+ T-cell
results. Tg-RAG mice were capable of eliciting ocular lesions in the absence of
detectable reactivity to viral antigens. Lesion manifestation in Tg-RAG
mice was CD4+ T-cell dependent and the cellular infiltrates
and their inflammatory products in the HSV-infected cornea were
comparable to similarly infected BALB/c and DO11.10 mice.
conclusions. The authors conclude that mechanisms other than viral antigen
recognition, and hence molecular mimicry, are at play and are
sufficient to cause HSV-induced stromal keratitis. The data imply a
significant role for non–virus-specific CD4+ T cells that
could become activated by an inflammatory milieu consisting of enhanced
accessory molecules and proinflammatory cytokines in the
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