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Scott K. Durum

Researcher at National Institutes of Health

Publications -  144
Citations -  10942

Scott K. Durum is an academic researcher from National Institutes of Health. The author has contributed to research in topics: T cell & Receptor. The author has an hindex of 53, co-authored 136 publications receiving 10110 citations. Previous affiliations of Scott K. Durum include Science Applications International Corporation.

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There is more than one interleukin 1.

TL;DR: The biochemical characteristics, gene cloning, cell sources, biological properties and actions of IL-1 are discussed, and reasons why this pleitotropic, nonspecific hormone-like cytokine is of considerable concern to immunologists are given.
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Interleukin-7 receptor expression: intelligent design

TL;DR: There is mounting evidence indicating that the amount of IL-7 receptor expressed on a cell not only determines how vigorously the cell responds toIL-7, but it can also determine how efficiently the cell consumes IL- 7 and, therefore, affect the supply of this limiting resource in the niche.
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Interleukin 1: an immunological perspective.

TL;DR: The immunological discovery of IL-l sprang from serendipitous findings during the course of early studies on suppressor T cells (Ts), when the possibility was being tested that Ts might suppress the mitogenic response of T cells stimulated by phytohemagglutinin (PHA).
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Th17 Cells Are Long Lived and Retain a Stem Cell-like Molecular Signature

TL;DR: Th17 cells, despite displaying low expression of CD27 and other phenotypic markers of terminal differentiation, efficiently eradicated tumors and caused autoimmunity, were long lived, and maintained a core molecular signature resembling early memory CD8(+) cells with stem cell-like properties.
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Stat5a/b are essential for normal lymphoid development and differentiation

TL;DR: It is shown that mice completely deficient in Stat5a/b have severely impaired lymphoid development and differentiation and results in severe combined immunodeficiency, similar in many respects to deficiency of IL-7R, gammac, and Jak3.