A T cell line (designated C6.9-VP2) was isolated from the spinal cords of Theiler's murine encephalomyelitis virus (TMEV, BeAn strain) infected SJL/J mice that specifically recognizes the TMEV capsid protein peptide VP2<sub>74-86</sub>. Based on this cell line, a transgenic strain that expresses the VP2-specific regulatory T cell receptor was created on the SJL/J genetic background. Hemizygotes are viable and fertile. Compared to expression of the transgene in the resistant B6 background, these SJL/J mice exhibit a 2-fold increase of CD4+ T cells, with a decrease in CD8+ positive T cells and a 2- to 3- fold decrease in CD4+/CD8+ double positive T cells in the central nervous system (CNS) in response to TMEV infection.  Expression of the transgene on CD4+ T cells in this susceptible background enhances Th17 responses and subsequent Interleukin (IL)-17 secretion, thus promoting viral persistence and replication by inhibiting virus-induced cell apoptosis.   Unrestricted viral infection activates harmful immune responses which lead to demyelination disease.  Treatment of these mice with anti-IL-17 antibodies in conjunction with TMEV infection enhances viral clearance and inhibits the development of demyelination disease.  Infection of TCR VP2 mice with TMEV results in an accelerated development of demyelinating disease.

This transgenic mouse expressed the TMEV capsid protein peptide, VP2<sub>74-86</sub>, specific regulatory T cell receptor. These mice are useful for studying Th17 responses to  viral infection and subsequent inflammatory diseases.

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