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By B Kyewski

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2001; Walker et al. 2003a). In one well-characterized model, a high level of peptide expression resulted in the deletion of TCR transgenic T cells, whereas a moderate level resulted in partial deletion, with the development of CD25+ cells resembling TR in approximately 50% of the remaining cells (Jordan et al. 2001). Thus, these data serve as a direct demonstration that regulatory T cells could develop due to interactions with self-peptide:MHC complexes. Where does this TCR interaction with antigen occur?

40 Abstract CD25+ CD4+ T cells (TR ) are a naturally arising subset of regulatory T cells important for the preservation of self-tolerance and the prevention of autoimmunity. Although there is substantial data that TCR specificity is important for TR development and function, relatively little is known about the antigen specificity of naturally arising TR . Here, we will review the available evidence regarding naturally arising TR TCR specificity in the context of TR development, function, and homeostasis.

Rudensky not observed in TCR transgenic mice lacking RAG genes (Hori et al. 2002; Itoh et al. 1999, Olivares-Villagomes et al. 1998). The presence of functional RAG genes does permit the development of CD25+ TR in TCR transgenic mice, presumably via expression of endogenously rearranged TCR chains. The likely explanation for the lack of CD25+ T cell development in these monoclonal TCR transgenic mice is that the transgenic CD4+ TCRs reported so far most likely originated from CD25– T cells. This is inferred from the well-known inability of TR to proliferate or produce IL-2 in response to TCR engagement in vitro (Takahashi et al.

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