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• W2016377968 abstract "Summary Recent data suggest that many autoreactive T cells, particularly to tissue‐specific self antigens, can escape thymic deletion. The current dogma is that these autoreactive T cells are silenced by the failure of most tissues to provide co‐stimulation (signal 2), antigen alone (signal 1) inducing T cell unresponsiveness. However, I propose that activation of autoreactive T cells frequently occurs but autodestruction by effector T cells is tightly regulated. This phenomenon is most evident with lymph node metastasizing tumour cells where the regional lymph node can mount a vigorous response to the invading tumour cells but tumour growth is unimpaired. I suggest that autodestruction is prevented by inhibitory receptors on T cells which recognize class I MHC structures on target cells. These receptors, which I propose deliver 'signal minus T to T cells, were recently described on NK cells and a subpopulation of peripheral T cells. They are also strikingly similar to a family of anti‐self receptors that my laboratory described on murine T and B cells 15 years ago. In the ‘signal minus 1’model, antigen‐activated T cells acquire the inhibitory receptors when they become co‐stimulation independent and gain the ability to exit lymphoid organs and enter non‐lymphoid tissues. Thus, if autoreactive effector T cells encounter autoantigen in tissues they are functionally silenced by inhibitory receptor engagement and signal minus 1 delivery. In contrast, I propose that in response to intracellular infections, cells down‐regulate expression of their ligands for inhibitory receptors. Such a model allows infected cells to be selectively eliminated by effector T cells. If correct, the model predicts that effector T cells, whether foreign antigen‐ or autoantigen‐specific, can selectively respond to infected cells. This apparent‘usefulness’of autoreactive T cells may explain their observed persistence even after an encounter with autoantigen. It is also suggested that signal minus 1 may silence autoreactive B cells specific for tissue‐specific cell surface antigens and lack of signal minus 1 may partially explain the vigorous T cell response to allogeneic MHC. Finally, it is hypothesized that, in evolutionary’terms, inhibition of autodestruction by the recognition of a 'self marker’and delivery of signal minus 1 is an ancient process which probably emerged in early metazoans." @default.
• W2016377968 created "2016-06-24" @default.
• W2016377968 creator A5068646165 @default.
• W2016377968 date "1996-06-01" @default.
• W2016377968 modified "2023-09-30" @default.
• W2016377968 title "Signal minus 1: A key factor in immunological tolerance to tissue-specific self antigens?" @default.
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• W2016377968 doi "https://doi.org/10.1038/icb.1996.49" @default.
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