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Nancy Noben-Trauth

Researcher at National Institutes of Health

Publications -  25
Citations -  4084

Nancy Noben-Trauth is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Interleukin 4 & T cell. The author has an hindex of 21, co-authored 25 publications receiving 3937 citations. Previous affiliations of Nancy Noben-Trauth include Government of the United States of America.

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NKT cell–mediated repression of tumor immunosurveillance by IL-13 and the IL-4R–STAT6 pathway

TL;DR: In this paper, the authors investigated the mechanisms for down-regulation of cytotoxic T lymphocyte-mediated tumor immunosurveillance using a mouse model in which tumors show a growth-regression-recurrence pattern.
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IL-13, IL-4Rα, and Stat6 Are Required for the Expulsion of the Gastrointestinal Nematode Parasite Nippostrongylus brasiliensis

TL;DR: It is demonstrated that Stat6 signaling is not required for IL-4 enhancement of IgG1 production and actually inhibits IL- 4-induction of mucosal mastocytosis, and IL-13 may be more important thanIL-4 as an inducer of the Stat6 signaled signaling that leads to worm expulsion.
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Development of a Natural Model of Cutaneous Leishmaniasis: Powerful Effects of Vector Saliva and Saliva Preexposure on the Long-Term Outcome of Leishmania major Infection in the Mouse Ear Dermis

TL;DR: The studies reveal a dramatic exacerbating effect of SGS on lesion development in the dermal site, and a complete abrogation of this effect in mice preexposed to salivary components, the first to suggest that for individuals at risk of vector-borne infections, history of exposure to vector saliva might influence the outcome of Exposure to transmitted parasites.
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IL-18 induction of IgE: dependence on CD4+ T cells, IL-4 and STAT6.

TL;DR: IL-18, an IL-1–like cytokine that requires cleavage with caspase-1 to become active, was found to increase IgE production in a CD4+ T cells−, IL-4– and STAT6–dependent fashion, providing a potential therapeutic target for allergic disorders.
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An interleukin 4 (IL-4)-independent pathway for CD4+ T cell IL-4 production is revealed in IL-4 receptor-deficient mice

TL;DR: Results indicate that an IL-4-independent, beta2-microglobulin-dependent pathway exists through which the CD62L-low CD4+ population has acquired IL- 4-producing capacity in vivo, strongly suggesting that these cells are NK T cells.