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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T-cell subsets: transcriptional control in the Th1/Th2 decision.
TL;DR: Transcriptional mechanisms in CD4+ T cells and antigen-presenting cells determine the activation or differentiation of Th1 and Th2 helper cell subsets, and also form attractive targets for therapeutic intervention in the balance of Th 1/Th2 responses as mentioned in this paper.
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Signaling by the JNK group of MAP kinases
TL;DR: Advances in understanding the expression, function, and regulation of the JNK pathway in T-lymphocyte activation and differentiation are summarized.
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A Role for Tumor Necrosis Factor Receptor Type 1 in Gut-associated Lymphoid Tissue Development: Genetic Evidence of Synergism with Lymphotoxin β
TL;DR: It is shown that mice made deficient in both LTβ and TNFR type 1 (TNFR1) lack all LNs, revealing redundancy or synergism between TNFR1 and LTβ, acting presumably via LTβR.
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Divergent Effects of miR-181 Family Members on Myocardial Function Through Protective Cytosolic and Detrimental Mitochondrial microRNA Targets
Samarjit Das,Mark J. Kohr,Brittany Dunkerly-Eyring,Dong I. Lee,Djahida Bedja,Djahida Bedja,Oliver A. Kent,Anthony K.L. Leung,Jorge Henao-Mejia,Richard A. Flavell,Charles Steenbergen +10 more
TL;DR: The miR‐181 family alters the myocardial response to oxidative stress, notably with detrimental effects by targeting mt‐COX1 (miR‐ 181c) or with protection by targeting PTEN (mi R‐181a/b).
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Multiple MyD88-dependent responses contribute to pulmonary clearance of Legionella pneumophila
TL;DR: The MyD88‐dependent innate immune responses induced by L. pneumophila involve both TLR‐dependent responses and IL‐18R‐ dependent production of IFN‐γ by natural killer cells, and these MyD 88‐dependent pathways can function independently to provide host protection against an intracellular pathogen.