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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Toll-like receptor 7 and TLR9 dictate autoantibody specificity and have opposing inflammatory and regulatory roles in a murine model of lupus.
Sean R. Christensen,Jonathan Shupe,Kevin M. Nickerson,Michael Kashgarian,Richard A. Flavell,Mark J. Shlomchik +5 more
TL;DR: It is reported that lupus-prone mice deficient in TLR7, a receptor for ssRNA, failed to generate Abs to RNA-containing antigens (Ags) such as Smith (Sm) Ag and TLR9, and this results have important implications for TLR-directed therapy of autoimmune disease.
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Infiltration of CD4+ lymphocytes into the brain contributes to neurodegeneration in a mouse model of Parkinson disease
Vanessa Brochard,Béhazine Combadière,Annick Prigent,Yasmina Laouar,Aline Perrin,Virginie Beray-Berthat,Olivia Bonduelle,Daniel Alvarez-Fischer,Jacques Callebert,Jean-Marie Launay,Charles Duyckaerts,Richard A. Flavell,Etienne C. Hirsch,Stéphane Hunot +13 more
TL;DR: It is shown that CD8+ and CD4+ T cells but not B cells had invaded the brain in both postmortem human PD specimens and in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of PD during the course of neuronal degeneration, and that MPTP-induced dopaminergic cell death was markedly attenuated in the absence of mature T lymphocytes.
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Abrogation of TGFβ Signaling in T Cells Leads to Spontaneous T Cell Differentiation and Autoimmune Disease
TL;DR: It is shown that T cell homeostasis requires T GFβ signaling in T cells, and a transgenic approach to abrogate the TGFβ response in key immune cells is developed.
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The Jnk1 and Jnk2 protein kinases are required for regional specific apoptosis during early brain development.
Chia-Yi Kuan,Derek D. Yang,Deborah R. Samanta Roy,Roger J. Davis,Pasko Rakic,Richard A. Flavell +5 more
TL;DR: It is suggested that Jnk1 andJnk2 regulate region-specific apoptosis during early brain development by reducing cell death in the lateral edges of hindbrain prior to neural tube closure and increasing apoptosis and caspase activation in the mutant forebrain.
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ICOS co-stimulatory receptor is essential for T-cell activation and function.
Chen Dong,Amy E. Juedes,Ulla Angela Temann,Ulla Angela Temann,Sujan Shresta,James P. Allison,Nancy H. Ruddle,Richard A. Flavell,Richard A. Flavell +8 more
TL;DR: It is shown that T-cell activation and proliferation are defective in the absence of ICOS, and ICOS-/- mice showed greatly enhanced susceptibility to experimental autoimmune encephalomyelitis, indicating that ICOS has a protective role in inflammatory autoimmune diseases.