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
ZPR1 is essential for survival and is required for localization of the survival motor neurons (SMN) protein to Cajal bodies
TL;DR: It is reported that targeted ablation of the Zpr1 gene in mice disrupts the subcellular localization of both SMN and spliceosomal snRNPs and indicates that ZPR1 contributes to the regulation of SMN complexes and that it is essential for cell survival.
Journal Article
Protective antibodies in murine Lyme disease arise independently of CD40 ligand.
TL;DR: Data show that B. burgdorferi-infected CD40L-deficient mice are capable of producing Abs that are protective, despite the inability of these mice to mediate T-dependent immune responses.
Journal ArticleDOI
The Role of Toll-Like Receptors 3 and 9 in the Development of Autoimmune Diabetes in NOD Mice
TL;DR: The results suggest that different TLRs play a varying role in autoimmune diseases, and NOD mice that are deficient in TLR3 and 9 were markedly protected from the disease compared to TLR9 heterozygous mice.
Journal Article
alpha beta T cell regulation and CD40 ligand dependence in murine systemic autoimmunity.
Stanford L. Peng,Jennifer M. McNiff,Michael P. Madaio,Jian Ma,Michael J. Owen,Richard A. Flavell,Adrian Hayday,Joe Craft +7 more
TL;DR: Disruption of CD40L and alpha beta T cells provides a novel dissection of the physiology and pathology of murine lupus and suggests a role for alphabeta T cells in the down-regulation of autoimmunity driven by other T cells.
The Presumptive Phosphatidylserine Receptor Is Dispensable for Innate Anti-inflammatory Recognition and Clearance of
Justin E. Mitchell,Marija Cvetanovic,Nitu Tibrewal,Vimal A. Patel,Oscar R. Colamonici,Ming O. Li,Richard A. Flavell,Jerrold S. Levine,Raymond B. Birge,David S. Ucker +9 more
TL;DR: It is concluded that PSR is not involved generally in either specific innate recognition or engulfment of apoptotic cells, and does not play a role in pro-inflammatory transcription or in the anti-inflammatory modulation of that transcriptional response triggered by apoptosis.