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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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How Diverse—CD4 Effector T Cells and their Functions

TL;DR: This review will discuss the classification and immunological functions of effector T cells, the determinants for effectors T cell differentiation, as well as the relationship between different lineages of effectors and the establishment of the Th1-Th2 dogma.
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Interleukin-13 mediates a fundamental pathway for airway epithelial mucus induced by CD4 T cells and interleukin-9.

TL;DR: In vivo pathways that lead to mucus induction are defined and indicate that, whereas IL-13 mediates a dominant pathway for CD4 Th induced inflammation, other inflammatory stimuli activate the epithelium to produce mucus by different pathways.
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The invariant chain is required for intracellular transport and function of major histocompatibility complex class II molecules.

TL;DR: The role of Ii chain is defined as a chaperone that assists class II during folding, assembly, and transport and causes them to be recognized as "misfolded" and retained in the same compartments as bona fide misfolded proteins.
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Impaired membrane resealing and autoimmune myositis in synaptotagmin VII–deficient mice

TL;DR: It is shown that embryonic fibroblasts from Syt VII–deficient mice are less susceptible to trypanosome invasion, and defective in lysosomal exocytosis and resealing after wounding, which suggests defective plasma membrane repair in tissues under mechanical stress may favor the development of inflammatory autoimmune disease.
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Virus Binding to a Plasma Membrane Receptor Triggers Interleukin-1α-Mediated Proinflammatory Macrophage Response In Vivo

TL;DR: Evidence is presented that macrophages in vivo activated an innate immune response to a double-stranded DNA virus, adenovirus (Ad), independently of TLR9 or NLRP3 inflammasome, identifying IL-1 alpha-IL-1RI as a key pathway allowing for the activation of proinflammatory responses to the virus, independently of its genomic nucleic acid recognition.