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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.

Papers
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ICOS-dependent extrafollicular helper T cells elicit IgG production via IL-21 in systemic autoimmunity.

Jared M. Odegard, +7 more
- 24 Nov 2008 - 
TL;DR: An anatomically distinct extrafollicular population of cells that regulates plasma cell differentiation in chronic autoimmunity is defined, indicating that specialized humoral effector T cells akin to TFH cells can occur outside the follicle.
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Regulation of IL-4 expression by the transcription factor JunB during T helper cell differentiation.

Baiyong Li, +3 more
- 15 Jan 1999 - 
TL;DR: It is shown that the early increase of JunB protein in Th2 cells can provide the specificity for c‐Maf in IL‐4 expression during T cell development and directs thereby Th2 differentiation.
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MKK7 is an essential component of the JNK signal transduction pathway activated by proinflammatory cytokines

Cathy Tournier, +5 more
- 01 Jun 2001 - 
TL;DR: It is shown that MKK4 and MKK7 serve different functions in the JNK signal transduction pathway, and disruption of the Mkk7 gene alone was sufficient to prevent JNK activation caused by proinflammatory cytokines.
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Dynamic signaling by T follicular helper cells during germinal center B cell selection

Ziv Shulman, +9 more
- 29 Aug 2014 - 
TL;DR: Using intravital imaging, it is found that selection is mediated by large but transient contacts between TFH and GC B cells presenting the highest levels of cognate peptide bound to major histocompatibility complex II.
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Microglial Activation Resulting from CD40-CD40L Interaction After β-Amyloid Stimulation

Jun Tan, +8 more
- 17 Dec 1999 - 
TL;DR: CD40 expression was increased and abnormal tau phosphorylation was reduced in Tg APPsw animals deficient for CD40L, suggesting that the CD40-CD40L interaction is an early event in AD pathogenesis.