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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Journal ArticleDOI
Mice Lacking Endogenous IL-10–Producing Regulatory B Cells Develop Exacerbated Disease and Present with an Increased Frequency of Th1/Th17 but a Decrease in Regulatory T Cells
Natalie A. Carter,Rita Vasconcellos,Elizabeth C. Rosser,Calogero Tulone,Alba Muñoz-Suano,Masahito Kamanaka,Masahito Kamanaka,Michael R. Ehrenstein,Richard A. Flavell,Claudia Mauri +9 more
TL;DR: It is reported that chimeric mice specifically lacking IL-10–producing B cells (IL-10−/−B cell) developed an exacerbated arthritis compared with chimeric wild-type (WT) B cell mice.
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A critical role of neural-specific JNK3 for ischemic apoptosis.
Chia-Yi Kuan,Alan J. Whitmarsh,Alan J. Whitmarsh,Derek D. Yang,Derek D. Yang,Guanghong Liao,Aryn Schloemer,Chen Dong,Jue Bao,Kenneth J. Banasiak,Kenneth J. Banasiak,Gabriel G. Haddad,Gabriel G. Haddad,Richard A. Flavell,Roger J. Davis,Pasko Rakic +15 more
TL;DR: It is shown that JNK1 is the major isoform responsible for the high level of basal JNK activity in the brain, and targeted deletion of Jnk3 not only reduces the stress-induced J NK activity, but also protects mice from brain injury after cerebral ischemia–hypoxia.
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JNK-mediated induction of cyclooxygenase 2 is required for neurodegeneration in a mouse model of Parkinson's disease
Stéphane Hunot,Miquel Vila,Peter Teismann,Roger J. Davis,Etienne C. Hirsch,Serge Przedborski,Pasko Rakic,Richard A. Flavell +7 more
TL;DR: By eliminating c-Jun N-terminal kinases (JNKs) the authors can prevent neurodegeneration and improve motor function in an animal model of PD, and revealed that JNK2- and JNK3-induced COX-2 may be a principle pathway responsible for neurodegenersation in PD.
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Direct Regulation of Gata3 Expression Determines the T Helper Differentiation Potential of Notch
Derk Amsen,Andrey Antov,Dragana Jankovic,Alan Sher,Freddy Radtke,Abdallah Souabni,Meinrad Busslinger,Brent McCright,Thomas Gridley,Richard A. Flavell +9 more
TL;DR: It is shown here that Notch was required on CD4(+) T cells for physiological Th2 responses to parasite antigens and Gata3 is a critical element determining inductive Th2 differentiation and limiting Th1 differentiation by Notch.
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Transforming growth factor-beta controls T helper type 1 cell development through regulation of natural killer cell interferon-gamma.
Yasmina Laouar,Fayyaz S. Sutterwala,Leonid Gorelik,Leonid Gorelik,Richard A. Flavell,Richard A. Flavell +5 more
TL;DR: It is shown that transforming growth factor-β (TGF-β) controlled TH1 differentiation through the regulation of interferon-γ produced by natural killer (NK) cells, indicating a previously undescribed demarcation of the function of TGF- β in NK cells versus dendritic cells.