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Kate L. Jeffrey

Researcher at Harvard University

Publications -  34
Citations -  4494

Kate L. Jeffrey is an academic researcher from Harvard University. The author has contributed to research in topics: Epigenetics & Innate immune system. The author has an hindex of 16, co-authored 28 publications receiving 3625 citations. Previous affiliations of Kate L. Jeffrey include Rockefeller University & Massachusetts Institute of Technology.

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Suppression of inflammation by a synthetic histone mimic

TL;DR: A synthetic compound (I-BET) is described that by ‘mimicking’ acetylated histones disrupts chromatin complexes responsible for the expression of key inflammatory genes in activated macrophages, and confers protection against lipopolysaccharide-induced endotoxic shock and bacteria-induced sepsis.
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Microbial stimulation fully differentiates monocytes to DC-SIGN/CD209+ dendritic cells for immune T cell areas

TL;DR: It is shown that fully differentiated monocyte-derived DCs (Mo-DCs) develop in mice and DC-SIGN/CD209a marks the cells, and the blood monocyte reservoir becomes the dominant presenting cell in response to select microbes, yielding DC- SIGN(+) cells with critical functions of DCs.
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Targeting dual-specificity phosphatases: manipulating MAP kinase signalling and immune responses

TL;DR: From a drug discovery perspective, DUSP family members are promising drug targets for manipulating MAPK-dependent immune responses in a cell-type and disease-context-dependent manner, to either boost or subdueimmune responses in cancers, infectious diseases or inflammatory disorders.
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Conserved vertebrate mir-451 provides a platform for Dicer-independent, Ago2-mediated microRNA biogenesis

TL;DR: It is shown that maturation of miR-451, a functional miRNA that is perfectly conserved among vertebrates, is independent of Dicer, and the mir-451 backbone is amenable to reprogramming, permitting vector-driven expression of diverse functional miRNAs in the absence of Dacer.
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Suppression of the antiviral response by an influenza histone mimic

TL;DR: It is proposed that the histone mimic in NS1 enables the influenza virus to affect inducible gene expression selectively, thus contributing to suppression of the antiviral response.