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Stephanie S. Watowich

Researcher at University of Texas MD Anderson Cancer Center

Publications -  129
Citations -  16730

Stephanie S. Watowich is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Signal transduction & Cellular differentiation. The author has an hindex of 48, co-authored 113 publications receiving 14947 citations. Previous affiliations of Stephanie S. Watowich include University of Texas Health Science Center at Houston & Northwestern University.

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T Helper 17 Lineage Differentiation Is Programmed by Orphan Nuclear Receptors RORα and RORγ

TL;DR: Th17 differentiation is directed by two lineage-specific nuclear receptors, ROR alpha and ROR gamma, and is induced by transforming growth factor-beta and interleukin-6 (IL-6), which is dependent on signal transducer and activator of transcription 3.
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Essential autocrine regulation by IL-21 in the generation of inflammatory T cells

TL;DR: IL-21 is shown to be an autocrine cytokine that is sufficient and necessary for TH17 differentiation, and serves as a target for treating inflammatory diseases.
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Stat3 regulates cytokine-mediated generation of inflammatory helper t cells

TL;DR: A pathway whereby cytokines regulate THi differentiation through a selective STAT transcription factor that functions to regulate lineage-specific gene expression is demonstrated.
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Generation of T Follicular Helper Cells Is Mediated by Interleukin-21 but Independent of T Helper 1, 2, or 17 Cell Lineages

TL;DR: It is shown that Tfh cells had a distinct gene expression profile and developed in vivo independently of the Th1 or Th2 cell lineages and was dependent on interleukin-21 (IL-21), IL-6, and signal transducer and activator of transcription 3 (STAT3) in vivo.
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Critical Regulation of Early Th17 Cell Differentiation by Interleukin-1 Signaling

TL;DR: It is shown that interleukin-1 (IL-1) signaling on T cells is critically required for the early programming of Th 17 cell lineage and Th17 cell-mediated autoimmunity and this pathway may serve as a unique target for Th17cell-mediated immunopathology.