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David L. Williams

Researcher at East Tennessee State University James H. Quillen College of Medicine

Publications -  113
Citations -  11454

David L. Williams is an academic researcher from East Tennessee State University James H. Quillen College of Medicine. The author has contributed to research in topics: Glucan & Innate immune system. The author has an hindex of 52, co-authored 111 publications receiving 10569 citations. Previous affiliations of David L. Williams include Tulane University & East Tennessee State University.

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Dectin-1 Mediates the Biological Effects of β-Glucans

TL;DR: It is shown that Dectin-1 mediates the production of TNF-α in response to zymosan and live fungal pathogens, an activity that occurs at the cell surface and requires the cytoplasmic tail and immunoreceptor tyrosine activation motif of Dect in addition to Toll-like receptor (TLR)-2 and Myd88.
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Dectin-1 Is A Major β-Glucan Receptor On Macrophages

TL;DR: Dectin-1 is defined as the leukocyte β-glucan receptor, first described over 50 years ago, and resolves the long-standing controversy regarding the identity of this important molecule, which is identified as a new target for examining the immunomodulatory properties of β- glucans for therapeutic drug design.
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Syk-Dependent Cytokine Induction by Dectin-1 Reveals a Novel Pattern Recognition Pathway for C Type Lectins

TL;DR: It is demonstrated that the beta-glucan receptor Dectin-1, a yeast binding C type lectin known to synergize with TLR2 to induce TNF alpha and IL-12, can also promote synthesis of IL-2 andIL-10 through phosphorylation of the membrane proximal tyrosine in the cytoplasmic domain and recruitment of Syk kinase.
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The Beta-Glucan Receptor Dectin-1 Recognizes Specific Morphologies of Aspergillus fumigatus

TL;DR: Data show that dectin-1 is centrally required for the generation of alveolar macrophage proinflammatory responses to A. fumigatus and provides the first in vivo evidence for the role of dectIn-1 in fungal innate defense.