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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Impairment of antigen-specific T-cell priming in mice lacking CD40 ligand.
TL;DR: Adoptively transferred antigen-specific CD4+ T cells lacking CD40L failed to expand upon antigen challenge of the recipients, showing that expression ofCD40L on T cells is required for in vivo priming of CD4 + T cells and therefore for the initiation of specific T-cell immune responses.
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Control of Toll-like Receptor 7 Expression Is Essential to Restrict Autoimmunity and Dendritic Cell Proliferation
Jonathan A. Deane,Prapaporn Pisitkun,Rebecca S. Barrett,Lionel Feigenbaum,Terrence Town,Jerrold M. Ward,Richard A. Flavell,Silvia Bolland +7 more
TL;DR: It is demonstrated that duplication of the Tlr7 gene was the sole requirement for this accelerated autoimmunity, because reduction of TLR7 gene dosage abolished the Yaa phenotype.
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Mechanism of p38 MAP kinase activation in vivo
Deborah Marie Brancho,Nobuyuki Tanaka,Anja Jaeschke,Juan-Jose Ventura,Nyaya Kelkar,Yoshinori Tanaka,Masanao Kyuuma,Toshikazu Takeshita,Richard A. Flavell,Roger J. Davis +9 more
TL;DR: It is shown that MKK3 and MKK6 are essential for tumor necrosis factor-stimulated p38 MAPK activation, and loss of p38MAPK activation in the mutant cells was associated with defects in growth arrest and increased tumorigenesis.
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Protection of mice against the Lyme disease agent by immunizing with recombinant OspA
TL;DR: C3H/HeJ mice actively immunized with live transformed E. coli or purified recombinant OspA protein produced antibodies to OSpA and were protected from challenge with several strains of B. burgdorferi.
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The Role of Fas in Autoimmune Diabetes
Alexander V. Chervonsky,Yi Wang,F. Susan Wong,Irene Visintin,Richard A. Flavell,Richard A. Flavell,Charles A. Janeway,Charles A. Janeway,Louis A. Matis +8 more
TL;DR: Induction of Fas expression on beta cells and their subsequent destruction constitutes the main pathogenic mechanism in autoimmune diabetes.