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Richard A. Flavell

Researcher at Yale University

Publications -  1389
Citations -  223064

Richard A. Flavell is an academic researcher from Yale University. The author has contributed to research in topics: Immune system & T cell. The author has an hindex of 231, co-authored 1328 publications receiving 205119 citations. Previous affiliations of Richard A. Flavell include National Institute for Medical Research & University of Michigan.

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The dual nature of T H 17 cells: shifting the focus to function

TL;DR: In this Perspective, critical differences between IL-17 itself and TH17 cells are highlighted and the protective nature of IL- 17 and Th17 cells is discussed.
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NALP3-mediated inflammation is a principal cause of progressive renal failure in oxalate nephropathy

TL;DR: Progressive renal failure in oxalate nephropathy results primarily from NALP3-mediated inflammation, thereby excluding differences in intestinal oxalates handling to explain the observed phenotype.
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Innate sensors of pathogen and stress: linking inflammation to obesity.

TL;DR: Recent studies demonstrating the important roles of innate pathogen receptors, including Toll-like receptors, nucleotide oligomerization domain containing proteins, and inflammasomes in mediating the inflammatory response to metabolic stress in different tissues are summarized and the interaction of innate pattern recognition receptors, gut microbiota, and nutrients are highlighted.
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Opposing Effects of TGF-β and IL-15 Cytokines Control the Number of Short-Lived Effector CD8+ T Cells

TL;DR: It is demonstrated that the number of effector CD8(+) T cells is tightly controlled by multiple extrinsic signals throughout effector differentiation; this plasticity should be exploited during vaccine design and immunotherapy against tumors and autoimmune diseases.
Journal Article

Human IL-3/GM-CSF knock-in mice support human alveolar macrophage development and human immune responses in the lung

TL;DR: In this article, the authors used human IL-3/GM-CSF knock-in mice to study the human myeloid cell reconstitution in the lung and showed that these mice supported the development of human alveolar macrophages that partially rescued the pulmonary alveoral proteinosis syndrome.