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Megan A. Cooper

Researcher at Washington University in St. Louis

Publications -  116
Citations -  12314

Megan A. Cooper is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Medicine & Immune system. The author has an hindex of 36, co-authored 89 publications receiving 10466 citations. Previous affiliations of Megan A. Cooper include Harvard University & St. Louis Children's Hospital.

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The biology of human natural killer-cell subsets.

TL;DR: Human natural killer cells comprise approximately 15% of all circulating lymphocytes and have the capacity to produce abundant cytokines following activation of monocytes, but has low natural cytotoxicity and is CD16(dim) or CD16(-).
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Human natural killer cells: a unique innate immunoregulatory role for the CD56bright subset

TL;DR: It is proposed that human CD56bright NK cells have a unique functional role in the innate immune response as the primary source of NK cell–derived immunoregulatory cytokines, regulated in part by differential monokine production.
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CD56bright natural killer cells are present in human lymph nodes and are activated by T cell–derived IL-2: a potential new link between adaptive and innate immunity

TL;DR: It is demonstrated that CD56(bright) NK cells are present in human lymph nodes and that endogenous T cell-derived IL-2, acting through the NK high-affinityIL-2 receptor, costimulates CD56 (bright)NK cells to secrete IFN-gamma.
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Cytokine-induced memory-like natural killer cells

TL;DR: It is shown that cytokine-activated NK cells transferred into naïve hosts can be specifically detected 7–22 days later when they are phenotypically similar to naïve cells and are not constitutively producing IFN-γ, indicating an ability of innate immune cells to retain an intrinsic memory of prior activation.
Journal Article

Differential Cytokine and Chemokine Gene Expression by Human NK Cells Following Activation with IL-18 or IL-15 in Combination with IL-12: Implications for the Innate Immune Response

TL;DR: The results show that distinct cytokine and chemokine patterns are induced in NK cells in response to different costimulatory signals from these three monokines, which suggests that NK cell cytokine production may be governed in part by the monokine milieu induced during the early proinflammatory response to infection and by the subset of NK cells present at the site of inflammation.