R
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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Cycloheximide, an inhibitor of protein synthesis, prevents γ-interferon-induced expression of class II mRNA in a macrophage cell line
TL;DR: The studies suggest that this putative protein factor is labile and required throughout the induction period, and nuclear run-off assays demonstrate that IFN-γ induces class II mRNA at the transcriptional level.
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The missing link: how the inflammasome senses oxidative stress
TL;DR: It is found that thio-redoxin (TRX)-interacting protein (TXNIP) can bind to NLRP3, the key in AMmasomecomponent in a reactive oxygen species(ROS)-responsive manner, thus elucidating the link between ROS production and AMM activation.
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IL‐12/23p40‐dependent clearance of Anaplasma phagocytophilum in the murine model of human anaplasmosis
Joao H. F. Pedra,Jian Tao,Fayyaz S. Sutterwala,Bindu Sukumaran,Nancy Berliner,Linda K. Bockenstedt,Richard A. Flavell,Richard A. Flavell,Zhinan Yin,Erol Fikrig +9 more
TL;DR: The data suggest that the immune response against A. phagocytophilum is a multifactorial and cooperative process and IL-12/23p40-independent mechanisms ultimately contribute to pathogen elimination from the host.
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Adaptive and Innate Transforming Growth Factor β Signaling Impact Herpes Simplex Virus 1 Latency and Reactivation
Sariah J. Allen,Kevin R. Mott,Steven L. Wechsler,Richard A. Flavell,Terrence Town,Homayon Ghiasi +5 more
TL;DR: Findings strongly suggest that TGF-β signaling, which generally functions to dampen immune responses, results in increased HSV-1 latency.
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The induction and function of the anti-inflammatory fate of TH17 cells
Hao Xu,Theodora Agalioti,Jun Zhao,Babett Steglich,Ramez Wahib,Maria Carolina Amezcua Vesely,Piotr Bielecki,Will Bailis,Will Bailis,Ruaidhri Jackson,Daniel Perez,Jakob R. Izbicki,Paula Licona-Limón,Vesa Kaartinen,Jens Geginat,Enric Esplugues,Eva Tolosa,Samuel Huber,Richard A. Flavell,Nicola Gagliani,Nicola Gagliani +20 more
TL;DR: The capacity of TH17 cells to acquire an anti- inflammatory fate is necessary to sustain immunological tolerance, yet it impairs immune protection against S. aureus, and it is found that TGF-β signalling via Smad3/Smad4 is sufficient for the expression of the anti-inflammatory cytokine, IL-10, in TH 17 cells.