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Thomas A. Wynn

Researcher at University of California, San Diego

Publications -  300
Citations -  61781

Thomas A. Wynn is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Cytokine & Schistosoma mansoni. The author has an hindex of 111, co-authored 276 publications receiving 52854 citations. Previous affiliations of Thomas A. Wynn include Los Alamos National Laboratory & Urbana University.

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The adaptor protein CIKS/Act1 is essential for IL-25-mediated allergic airway inflammation.

TL;DR: It is demonstrated that IL-25 can initiate an allergic asthma-like inflammation in the airways, which includes recruitment of eosinophils, mucus hypersecretion, Th2 cytokine production, and airways hyperreactivity, which is entirely dependent on the adaptor protein CIKS (also known as Act1).
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Combinatorial targeting of TSLP, IL-25, and IL-33 in type 2 cytokine–driven inflammation and fibrosis

TL;DR: Combined blockade of TSLP, IL-25, and IL-33 may be needed to treat some forms of progressive inflammation and fibrosis and it is suggested that in some settings, early combined targeting of these mediators is necessary to ameliorate progressive type 2–driven disease.
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IL-13 receptor α 2 down-modulates granulomatous inflammation and prolongs host survival in schistosomiasis

TL;DR: It is shown that the IL-13 receptor alpha 2 (IL-13R alpha 2) is a critical mediator of immune down-modulation, identifying the receptor as a life-sustaining off signal for chronic and pernicious inflammation in schistosomiasis.
Journal Article

Optimal vaccination against Schistosoma mansoni requires the induction of both B cell- and IFN-gamma-dependent effector mechanisms.

TL;DR: It is indicated that effective vaccination against schistosomes depends on the simultaneous induction of both humoral and cell-mediated immunity, a conclusion that may explain the limited success of most subunit vaccine protocols designed to preferentially induce either B cell- or IFN-gamma-dependent protective mechanisms.
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The TNF-family cytokine TL1A drives IL-13-dependent small intestinal inflammation

TL;DR: A novel link between TL1A and interleukin 13 (IL-13) responses that results in small intestinal inflammation is established, and it is established thatTL1A–DR3 interactions are necessary and sufficient for T cell-dependent IBD.