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
A mouse model for the human pathogen Salmonella typhi.
Jeongmin Song,Tim Willinger,Anthony Rongvaux,Elizabeth E. Eynon,Sean Stevens,Markus G. Manz,Richard A. Flavell,Jorge E. Galán +7 more
TL;DR: It is found that immunodeficient Rag2(-/-) γc (-/-) mice engrafted with human fetal liver hematopoietic stem and progenitor cells are able to support S. Typhi replication and persistent infection.
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DNA sequences required for regulated expression of β-globin genes in murine erythroleukemia cells
TL;DR: It is suggested that DNA sequences that regulate beta-globin gene transcription during MEL differentiation are located both 5' and 3' to the translation initiation site.
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TGF-β and Regulatory T Cell in Immunity and Autoimmunity
TL;DR: The role of regulatory T cells and TGF-β in the control of immunity and autoimmunity and the mechanisms that underlie how these molecules control these responses are discussed.
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Estrogen prevents bone loss through transforming growth factor β signaling in T cells
Yuhao Gao,Wei-Ping Qian,Kimberly Dark,Gianluca Toraldo,Angela S.P. Lin,Robert E. Guldberg,Richard A. Flavell,M. Neale Weitzmann,Roberto Pacifici +8 more
TL;DR: It is shown that mice with T cell-specific blockade of type beta transforming growth factor (TGFbeta) signaling are completely insensitive to the bone-sparing effect of E, and that TGFbeta signaling in T cells preserves bone homeostasis by blunting T cell activation.
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Toll-like receptor 3 is an essential component of the innate stress response in virus-induced cardiac injury
Hordur S. Hardarson,J. Scott Baker,Zhao Yang,Enkhsaikhan Purevjav,Chien-Hua Huang,Lena Alexopoulou,Na Li,Richard A. Flavell,Neil E. Bowles,Jesus G. Vallejo +9 more
TL;DR: EMCV infection leads to a TLR3-dependent innate stress response, which is involved in mediating protection against virus-induced myocardial injury, and Histopathological examination showed that the inflammatory changes of the myocardium were less marked inTLR3(-/-) than in TLR 3(+/+)mice.