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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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Journal ArticleDOI

Improved regenerative myogenesis and muscular dystrophy in mice lacking Mkp5

TL;DR: Enhanced promyogenic MAPK activity preserved muscle stem cell function even in the absence of dystrophin and ultimately curtailed the pathogenesis associated with DMD, suggesting that MKP-5 may serve as a target to promote muscle stem Cell function in the treatment of degenerative skeletal muscle diseases.
Book ChapterDOI

The intestinal microbiota in chronic liver disease.

TL;DR: It is now evident that, during pathological processes associated with obesity, alcohol-intake, or autoimmunity, the interaction between these immune cell populations and the intestinal microbiota promotes chronic liver disease progression and therefore they represent a novel therapeutic target.
Journal ArticleDOI

Transforming Growth Factor-β Suppresses the Activation of CD8+ T-Cells When Naïve but Promotes Their Survival and Function Once Antigen Experienced : A Two-Faced Impact on Autoimmunity

TL;DR: When expressed selectively in the pancreas, TGF-β reduced apoptosis of differentiated autoreactive CD8+ T-cells, favoring their expansion and infiltration of the islets, highlighting a novel aspect of the pleiotropic nature of TGF, which has implications for the design of immune therapies involving this cytokine.
Journal ArticleDOI

Epigenetic and Transcriptional Programs Lead to Default IFN-γ Production by γδ T Cells

TL;DR: It is shown that the kinetics of IFN-γ transcription is faster in γδ T cells compared with CD4+ and CD8+ T cells and that γ Δ T cells produce significantly greater amounts of IFn-γ in a proliferation-independent manner when compared with other T cell subsets.