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Benedict Seddon

Researcher at University College London

Publications -  74
Citations -  4792

Benedict Seddon is an academic researcher from University College London. The author has contributed to research in topics: T cell & T-cell receptor. The author has an hindex of 31, co-authored 68 publications receiving 4262 citations. Previous affiliations of Benedict Seddon include Medical Research Council & University of Oxford.

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Interleukin 7 and T cell receptor signals regulate homeostasis of CD4 memory cells.

TL;DR: It is shown that interleukin 7 (IL-7) was an important survival factor for CD4 memory T cells that together with T cell receptor (TCR) signals regulated homeostasis of theCD4 memory population in lymphopenic conditions and in the intact immune system.
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The basic leucine zipper transcription factor E4BP4 is essential for natural killer cell development

TL;DR: Overexpression of E4bp4 was sufficient to increase NK cell production from hematopoietic progenitor cells and acted in a cell-intrinsic manner 'downstream' of the interleukin 15 receptor (IL-15R and through the transcription factor Id2.
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Peripheral Autoantigen Induces Regulatory T Cells that Prevent Autoimmunity

TL;DR: Data indicate that it is the peripheral autoantigen itself that stimulates the generation of the appropriate regulatory cells from thymic emigrant precursors, and significantly, in contrast to the peripheral CD4- T cells, CD4+CD8− thymocytes from 131I-treated PVG donors were still able to prevent thyroiditis upon adoptive transfer.
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Regulatory T Cells in the Control of Autoimmunity: the Essential Role of Transforming Growth Factor β and Interleukin 4 in the Prevention of Autoimmune Thyroiditis in Rats by Peripheral CD4+CD45RC− Cells and CD4+CD8− Thymocytes

TL;DR: It is shown that transforming growth factor (TGF)-β and interleukin (IL)-4 both play essential roles in the mechanism of this protection since administration of monoclonal antibodies that block the biological activity of either of these cytokines abrogates the protective effect of the donor cells in the recipient rats.
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The third function of the thymus

TL;DR: A T-cell-mediated mechanism that prevents the realization of this potential and how its failure can lead to the development of autoimmunity is described.