Why do effector T-cell responses persist?
A major challenge to our understanding of the pathogenesis of immune-mediated diseases is to elucidate why pathways of peripheral tolerance might fail. To this end, efforts have been invested in evaluating the number and function of regulatory cell subsets, in order to test the hypothesis that at sites of synovial inflammation there may be defects in pathways of peripheral tolerance. Studies have been thwarted to an extent because until recently the enumeration of subsets of naturally occurring regulatory T cells was based purely on CD4 and nonselective high level expression of the T-cell activation antigen CD25 (hereafter referred to as regulatory T cells [Tregs]). Even the inclusion of Foxp3 into the phenotyping armamentarium has not solved the problem, because this master transcription factor, which plays a central role in the function of Tregs [64] , is also induced upon TCR engagement of CD4+CD25- T cells [65] . Furthermore, there remains controversy as to whether there are genuin
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