Regulatory T cells are critical for the maintenance of peripheral tolerance. There is currently limited evidence in support of the existence and role of Treg memory, as memory has primarily been studied in effector T cell populations. The primary challenge in identifying Treg memory lies in the fact that most Tregs are thought to be self-antigen-specific. Because most of these self-antigens are constitutively expressed, it is difficult to study memory populations that persist in the absence of cognate antigen. Mice infected with the neurotropic strain of the murine coronavirus, mouse hepatitis virus (MHV), develop acute encephalitis as well as immune-mediated acute and chronic demyelinating diseases. Tregs recognizing the immunodominant epitope of MHV have been identified and shown to suppress T cell responses during MHV infection. These virus-specific Tregs play a role in ameliorating immunopathology in MHV infection, as adoptive transfers of Tregs prior to infection increase survival and reduce demyelination. Because MHV infection represents a scenario in which Tregs of known antigen-specificity encounter non-persistent cognate antigen, this represents an ideal model to study the development of Treg memory. Through the use of transgenic mice expressing a TCR specific for the immunodominant epitope of MHV, preliminary experiments suggest that adoptively transferred Tregs form memory populations. My work aims to characterize these cells in terms of function and gene expression, as well as to assess the stability of Foxp3 expression by these cells.

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